ATP5IF1 and lung carcinoma: Moreover, we have illustrated the differential phosphorylation of IF1 in: (i) the regulation of the metabolic flux of cancer cells that are forced into glycolysis or into OXPHOS, (ii) the transition into the OXPHOS-dependent and glycolytic-dependent phases of cells during their progression through the cell cycle, (iii) in the adaptation of the cells to hypoxia, and (iv) that the majority of IF1 is dephosphorylated, and hence active as an inhibitor of ATP synthase, in human breast, colon, and lung carcinomas [27].