In transgenic mice expressing anoxygen-stabilized isoform of HIF-1α, the cardiomyocytes exhibit markedreductions in SERCA 2a and ryanodine receptor 2 (RyR2) transcript levels [19].These functional RyR2 defects can increase in the release of systolicsarcoplasmic reticulum-derived Ca2+ together with abnormally elevatedcytosolic Ca2+ concentrations, leading to APD shortening and AF onset. The gene discussed is HIF1A; the disease is atrial fibrillation.