One study identified that primary and adaptive resistance to VEN-based therapy correlated with the acquisition or enrichment of different kinase-activating clones in AML, such as FLT3-ITD, FLT3-TKD, FLT3 N676K, and RAS mutations, whereas FLT3-ITD gain and TP53 loss were considered to account for the VEN resistance [133]. The gene discussed is FLT3; the disease is acute myeloid leukemia.