Recently, they have shown that in addition, high levels of the endogenous peptide inhibitor of the mitochondrial H+-ATP synthase, ATPase inhibitory factor 1 (IF1), are present in colon, lung, breast and ovarian carcinomas, possibly being another mechanism to inhibit still remaining H+-ATP synthase activity [10, 14]. The gene discussed is ATP5IF1; the disease is ovarian carcinoma.