Figure 3 summarizes the effect of IF1 dose on OSR in cancer and non-cancer cells when the mitochondrial content of IF1 is manipulated by its silencing, by knocking it out, or by its overexpression, both in transiently and stably transfected cells, as well as in primary neuronal cultures of genetically modified mouse models of loss- and gain-of-function of IF1 in the brain, clearly supporting a relevant inhibitory role for IF1 in ADP-stimulated mitochondrial respiration [2,3,5,7,9,11,12,23]. Here, ATP5IF1 is linked to cancer.