Due to fedratinib's significant GI side effect profile and the logistical difficulty of measuring thiamine levels, clinicians should proactively provide patients with thiamine supplements, anti-emetics, and anti-diarrheal therapies. Instructing patients to take the drug with food can also help mitigate GI toxicity.

BTK inhibitors function as highly potent antiplatelet agents, an 'on-target' effect. Many surgeons are unaware, leading to significant post-operative bleeding if the drug isn't stopped. Patients must be educated to inform their surgical teams and advocate for themselves.

Clinicians can reassure myelofibrosis patients that the drop in hemoglobin often seen when starting ruxolitinib does not carry the same negative prognostic weight as anemia caused by the disease itself. This distinction is crucial for managing patient expectations and continuing effective therapy despite initial side effects.

A diagnosis of myelofibrosis without a JAK2, CALR, or MPL mutation should be treated as a red flag, not a final diagnosis. It warrants a deeper investigation for alternative causes, such as MDS/MPN overlap syndromes or secondary fibrosis from other conditions like autoimmune disease or hairy cell leukemia.

While beneficial for patients with prior weight loss, ruxolitinib can cause significant weight gain (20-30 pounds) in other myelofibrosis patients. This quality-of-life issue should be discussed proactively, as it can become a major concern, effectively trading one disease state for another.

To combat the significant myelosuppression from the standard 28-day venetoclax cycle in AML, many clinicians are adopting a strategy of performing a bone marrow biopsy around day 21 and pausing the drug if blast clearance is achieved to allow for hematologic recovery.

While rereading pathology reports is always good practice, it provides the most clinical value in cases of suspected ET. These patients are frequently reclassified as having prefibrotic myelofibrosis, a diagnosis that significantly alters patient counseling, prognosis, and long-term management strategies.

For myelofibrosis patients with both anemia and splenomegaly, a practical approach is to start with ruxolitinib for its superior symptom control. If the subsequent anemia is not well-tolerated, switching to momelotinib allows for a more informed, personalized decision based on the patient's experience with both agents.

The development of new KIT inhibitors like bezuclastinib is largely fueled by the need for alternatives to high-dose avapritinib in advanced SM. Concerns about cognitive effects and rare intracranial hemorrhage with avapritinib create an opportunity for agents with less blood-brain barrier penetration.