Specifically, counteracting the binding of pro-apoptotic proteins with BH3-mimetics antagonizing BCL-2 (navitoclax and venetoclax) rather than MCL-1 (S63845) and/or BCL-XL (A1331852) abolishes this protected state (Fig. 5b), leading to increased apoptosis in FASN-inhibited cancer cells. The gene discussed is MCL1; the disease is cancer.