Since an increased tethering between mitochondria and the biggest internal Ca2+ store, the ER, was found in cancer cells [10], we hypothesize that cancer cells with high levels of PRMT1-driven methylation control their mitochondrial Ca2+ uptake via UCP2 to ensure suitable mitochondrial ATP production by stimulating dehydrogenases with a proper amount of Ca2+. The gene discussed is UCP2; the disease is cancer.