Although Tbx5 is expressed in the postnatal period, the major phenotype of adult mouse cardiomyocytes lacking Tbx5 is atrial fibrillation associated with downregulation of its ion channel target genes Nppa, Gja5, and Scn5a [59], suggesting that its role switches from predominately regulating proliferation in embryos to regulating conduction or homeostasis postnatally. The gene discussed is TBX5; the disease is atrial fibrillation.