For example, high rates of concomitant RUNX1 and SF3B1 alteration, but exclusivity for other common AML mutations (CEBPA bZIP in‐frame, NPM1, FLT3‐ITD), confirm recent findings for IKZF1N159S‐mutated AML and are consistent with transcriptomic‐based evidence for a rare molecular AML subtype within the AML‐MR group.6, 11. The gene discussed is SF3B1; the disease is acute myeloid leukemia.