ATP5IF1 and cancer: Our experiments in genetically modified mouse models of loss- and gain-of-function of IF1 support its function as an inhibitor of a fraction of mitochondrial ATP synthase under basal in vivo cellular conditions affecting metabolic reprograming, the activity of ATP synthase, ΔΨm and mtROS production, among other activities, as we previously demonstrated in cancer and non-cancer cells [2,3,23,30] and which was recently confirmed by an independent laboratory in a mouse model in heart [17].