Ablation of IF1 promoted an increase in oligomycin-sensitive rate of ATP synthesis in permeabilized cells, as assessed following the kinetics of the luminescence production of ATP (Fig. 1c), and in the ATP hydrolytic activity in isolated mitochondria (Fig. 1d), supporting the idea that a fraction of mitochondrial ATP synthase is inhibited by its binding to endogenous IF1 under basal cellular conditions of cancer cells. The gene discussed is ATP5IF1; the disease is cancer.