Given that venetoclax action converges on the mitochondria which actively participate in apoptosis, we monitored the mitochondrial potential after the thioridazine + venetoclax combined treatment, observing an exacerbation of the mitochondrial depolarization that resulted in high synergism of treatment, supporting the combination venetoclax + thioridazine as a useful strategy to be involved in further analyses for AML patients with KMT2A-AFDN fusion with either high BCL-2 or MCL-1 levels. The gene discussed is BCL2; the disease is acute myeloid leukemia.