Concerns over arterial events caused physicians to start CML patients on lower, less effective doses of ponatinib. Data shows a start-high (45mg) then reduce strategy is more effective for disease control and safely mitigates side effect risks, contrary to clinical practice.
The primary goal in CML is evolving from chronic management to achieving Treatment-Free Remission (TFR). This paradigm shift favors using the most potent TKIs, like asciminib, first-line to induce deep, rapid molecular responses and enable eventual therapy discontinuation.
Risk stratification in CML is moving beyond BCR-ABL. Additional mutations like ASXL1 are now known to predict poorer outcomes and reduced response to asciminib, while others like GATA2 are favorable, pushing for routine, broader genetic sequencing at diagnosis to personalize therapy.