Finally, the treatment landscape for AML has recently shifted to molecular targeted therapies, such as BLC2-inhibitors (venetoclax), FLT3 inhibitors (midostaurin, gilteritinib, quizartinib and sorafenib), CD33-directed antibodies (gemtuzumab ozogamicin) and IDH inhibitors (ivosidenib and enasidenib), rather than or in addition to cytotoxic chemotherapeutics or hypomethylating agents (HMAs). The gene discussed is FLT3; the disease is acute myeloid leukemia.