With regard to therapeutics, NPM1/cohesin-mut AML were more sensitive than NPM1-mut AML to EGFR inhibition, which may lead to the release of the differentiation brake [58] and to drugs targeting the tyrosine kinase receptor MET, likely due to a mild autocrine pathway activation in these cases, who express low levels of the ligand [59]. The gene discussed is MET; the disease is acute myeloid leukemia.