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Apoptotic evasion has been postulated as one of the main mechanisms of multiple myeloma (MM) cell survival.[1][1],[2][2] The intrinsic apoptotic pathway, tightly regulated by the BCL-2 protein family, is initiated by intracellularly sensed stress signals and ultimately leads to the permeabilization

Preclinical evaluation of the simultaneous inhibition of MCL-1 and BCL-2 with the combination of S63845 and venetoclax in multiple myeloma