Several studies have also shown that various FLT3 inhibitors (including midostaurin, quizartinib, and gilteritinib) increase BCL-2 dependence and reduce expression of BCL-xL and MCL-1, thereby synergistically inducing apoptosis and sensitizing FLT3-mutated AML cells to venetoclax [48, 51–53]. The gene discussed is MCL1; the disease is acute myeloid leukemia.