The MCL1 protein, highly overexpressed in many types of tumors, has so far been considered mainly as an anti-apoptotic factor from the Bcl-2 family, which prevents programmed cell death.[1][2] A new study has shown that MCL1 directly affects the central metabolic regulator mTORC1 and controls the bioenergetics of cancer cells.[1][2] It thus combines two classic characteristics of cancer – escape from apoptosis and impaired energy metabolism – into one molecular mechanism.[1][2] Researchers led by Dr. Mohamed Elgendy of the Mildred Scheel Early Career Center at the TUD Faculty of Medicine published the findings in Nature Communications.[1] MCL1 inhibitors in clinical development as anticancer drugs also inhibit mTOR signaling, which is of high clinical relevance because mTOR inhibitors are already routinely used in cancer therapy.[1][2] The study identified the molecular mechanism of the cardiotoxic side effects of these inhibitors and developed a dietary approach that significantly reduces them, which they confirmed in a humanized mouse model.[2] These discoveries expand the understanding of the role of MCL1 and open up new therapeutic possibilities.[1][2]