Gilteritinib (Gilt) combined with venetoclax (Ven) leads to proteasomal degradation of MCL-1, which overcomes venetoclax resistance in FLT3wt AML. Gilt and Ven combination dephosphorylates Extracellular signal Regulated Kinase (ERK), which induces phosphorylation of MCL-1 at serine 159 in FLT3wt AML cells. This leads to downregulation of MCL-1 caused by its proteosomal degradation. Professional illustration by Patrick Lane, ScEYEnce Studios.