Indeed, in human and animal models of heart failure and atrial fibrillation (AF), the increased expression of InsP3R2 (heart failure) and InsP3R1 (AF) in the nuclear/perinuclear regions was observed and associated elevated nuclear resting Ca2+ levels has been assumed to enhance activity of transcriptional factors that regulate pro-hypertrophic gene expression [46,56]. The gene discussed is ITPR1; the disease is heart failure.