MCL1 and neoplasm: In addition, data obtained on different solid tumors [31, 63, 64] showed that blockade of mTOR signaling and Bcl-2 activity triggered massive in vitro apoptosis by loss of mitochondrial membrane potential, activation of caspases and Mcl-1 downregulation and was highly synergistic in vivo providing tumor regressions without notable hematologic suppression.