In this paper, we provide evidence that (1) MAs have antileukemic activity, either in vitro or in vivo, in both AML and ALL, alone or in combination with chemotherapeutic drugs, (2) these effects depend on a complex modulation of both autophagy and intracellular signaling pathways regulating cell survival and apoptosis, and (3) are mediated by hERG1 channels. The gene discussed is KCNH2; the disease is acute myeloid leukemia.