When it binds to BCL2 within CLL cells, venetoclax liberates BH3-only proteins from BCL2 sequestration, inducing BCL2 homologous antagonist killer/BCL2 associated X (BAK/BAX) protein mediated mitochondrial permeabilisation and cellular apoptosis[35], independent of p53 function[36]. Here, BAX is linked to B-cell chronic lymphocytic leukemia.