Cardiac‐specific ATPIF1 deletion in mice prevents this metabolic switch, offering protection against chronic stress‐induced remodeling.[9a] Moreover, ATPIF1 has been shown to modulate apoptosis by interacting with pro‐apoptotic or anti‐apoptotic proteins, such as Bax, Bcl‐2, and Bcl‐xL.[9c] Furthermore, ATPIF1 proved to be involved in cancer by regulating the glycolytic switch, the Warburg effect, the tumor microenvironment, and the chemoresistance.[20]. The gene discussed is BAX; the disease is neoplasm.