Similar data were obtained in T-cell acute lymphoblastic leukemia (T-ALL), in which the combinations venetoclax/volasertib and venetoclax/onvasertib resulted in a synergistic interaction [78], and the mechanisms underlying the efficacy of the combination included the upregulation of BCL2 members (BL2L13 and NOXA) greatly favoring apoptosis [79]. The gene discussed is BCL2; the disease is T-cell acute lymphoblastic leukemia.