RYR2 and catecholaminergic polymorphic ventricular tachycardia: We previously demonstrated that the RyR2-H29D single-point mutation induces pathological post-translational modifications including PKA hyperphosphorylation at Ser2809, oxidation, S-nitrosylation and depletion of calstabin2, conferring a CPVT-like phenotype but under non-stress conditions [7].