PROTAC 21 possessed a unique mechanism of action (MOA) in inhibiting antiapoptotic BCL-2 proteins, i.e. potent degradation of BCL-XL and simultaneously enhanced inhibition of BCL-2, that enabled its high potency against BCL-XL dependent, BCL-2 dependent, and BCL-XL/BCL-2 dual-dependent cancer cells. This evidence concerns the gene BCL2L1 and cancer.