Fig. 7
Illustration of the mechanism in a schematic format. When abnormalities in the CEBPA gene (e.g., CEBPAbi) in AML cells cause conversion of C/EBPα-p42 to C/EBPα-p30 isoforms, excess C/EBPα-p30 reduces the dependence of AML cells on BCL2 and increases their dependence on other anti-apoptotic proteins, thereby making them resistant to venetoclax; The combination of ER stress inducers can overcome the resistance of AML cells with low C/EBPα p42/p30 ratio to venetoclax through MCL1 inhibition and cell cycle regulation