RYR2 and catecholaminergic polymorphic ventricular tachycardia: The Ca2+ transient decay was slower and more late Ca2+ sparks occurred in CaMKIIδc over-expressing mice than phospholamban knockout controls, which could be caused by RyR2 Ca2+ hypersensitivity, but could also be due to CaMKIIδc facilitation of ICa [132] that would also prolong the Ca2+ transient and promote late Ca2+ sparks [124] Liu et al. found abnormal Ca2+ release in ventricular myocytes from mice with the CPVT-causing CSQ2-R33Q mutation that results in a GoF RyR2 phenotype, suggesting systolic Ca2+ handling could also be affected by GoF mutations [133].