This research is something that will either matter quite a bit or not at all. Frankly, it’s premature at this point.
A team at King’s College Hospital in London just published a case report describing a patient who developed acute psychosis five months after starting ruxolitinib. Before we go any further, we need to establish what we’re actually dealing with here. A case report is one patient. It is, in the hierarchy of clinical evidence, roughly equivalent to your uncle saying he knew a guy once. This matters; remember it.
The Patient
The man was 40 when doctors diagnosed him with polycythemia vera, which is an “uncommon” blood cancer where your bone marrow decides to produce red blood cells with the enthusiasm of a college student who just discovered adderall. For 17 years, his doctors managed the condition with various treatments, including venesection (the British term for phlebotomy), hydroxyurea, and anagrelide.
Then his disease did what PV sometimes does. It progressed into myelofibrosis, a condition where scar tissue slowly replaces the spongy marrow inside your bones. His physicians started him on ruxolitinib, sold as Jakafi, which blocks the haywire JAK enzymes driving everything.
Five months later, the man stopped sleeping. Then came the paranoid delusions and auditory hallucinations. He was 60 years old, had never experienced a single psychiatric symptom in his life, had no family history of mental illness, did not drink excessively or use drugs. His brain scans came back clean, infection panels negative, and autoimmune workups unremarkable.
So they gave him antipsychotics, the psychosis persisted.
Three weeks into his hospitalization, somebody thought to stop the ruxolitinib.
Within seven days, he was himself again.
The Plausible Mechanism
The authors are not being reckless here. They acknowledge that ruxolitinib crosses the blood-brain barrier (most drugs do not) and influences several signaling pathways in the central nervous system, including something called the WNT pathway, which is involved in dopamine neurons. Dopamine dysfunction is basically the central character in the psychosis story. So the biological logic holds together.
There is also a prior case report documenting acute mania in a patient taking tofacitinib, a cousin drug in the JAK inhibitor family. Similar timeline with similar resolution after discontinuation.
Why You Should Remain Skeptical
This is one patient. Ruxolitinib has been prescribed to hundreds of thousands of people since 2011. If Jakafi side effects genuinely included psychosis with any meaningful frequency, we would have noticed by now. We would have more than a single case report from a London hospital published fifteen years after the drug’s approval.
The investigators, to their credit, admit significant limitations. They never performed an MRI of the brain. No lumbar puncture. No toxicology screen. The patient mentioned “work-related stress,” which the authors wave away but which any honest observer must acknowledge can trigger psychiatric breaks in vulnerable individuals.
The five-month gap between starting the medication and developing symptoms makes establishing causality difficult. The authors write that these observations “may be coincidental.” They are being appropriately humble, we should be too.
This is true of most research I read, by the way. Studies raise questions as often as they answer them. Opposing interpretations exist. Findings get challenged, revised, sometimes thrown out entirely. That is not a flaw in science; that is science.
What This Actually Means For You
For those currently taking ruxolitinib, any concerns about your treatment should go straight to your care team. They know your history. This case report creates a hypothesis. It does not confirm ruxolitinib psychosis as an established phenomenon. That would require large-scale pharmacovigilance studies examining thousands of patients, and those do not yet exist.
What you should do is pay attention. If you notice unusual changes in your thinking, mood, or perception, tell your doctor. That advice applies regardless of what medications you take.
And here is something every patient should do, because it matters: track your symptoms. Write them down. Note when they started, how long they lasted, and what made them better or worse. Then bring that information to your physician. Have the conversation. Your doctor cannot address what they do not know about, and you are the only expert on what is happening inside your own body.
We will continue following this story as more evidence emerges. For now, file this under “interesting, possibly important, definitely not proven.”
Reference
Potter LJ, Shetty S, Ceesay MM. Acute psychosis following initiation of ruxolitinib in post-polycythaemia vera myelofibrosis case report. Annals of Hematology. 2026;105:53. doi:10.1007/s00277-026-06764-0
Medical Disclaimer
This article is provided for educational and informational purposes only and is not intended as medical advice. It does not replace consultation with a qualified healthcare professional. Diagnosis, treatment decisions, and care plans should always be made in consultation with your physician or an appropriate MPN specialist who is familiar with your individual medical history.
by David Wallace, MPN Patient Advocate
