Mice with gain-of-function RyR2 mutations causing catecholaminergic polymorphic ventricular tachycardia (CPVT), and mice lacking the RyR2-stabilizing subunit FKBP12.6, develop Ca2+-handling abnormalities including increased SR Ca2+-leak and spontaneous SR Ca2+-release events (i.e., sparks, waves). The gene discussed is FKBP1B; the disease is catecholaminergic polymorphic ventricular tachycardia.