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FLT3-ITD mutation causes an increased level of BCL-xL and MCL-1 via activation of downstream PI3K-AKT, RAS-MAPK, and STAT5 pathways. AKT and ERK promoted inhibitory phosphorylation of GSK3, leading to a reduction of MCL1 ubiquitination and degradation. In addition to upregulation of MCL-1 and BCL-xL, STAT5 also increases MCL-1 indirectly through AKT activation. In summary, FLT3-ITD mutation confers Venetoclax resistance by upregulation of BCL-xL and MCL-1[48-53].
