The type 2 ryanodine receptor (RyR2) is the Ca2+ release channel on cardiac sarcoplasmic reticulum and plays a crucial role in cardiac E-C coupling. The mutations in RyR2 have been implicated in a number of arrhythmogenic disorders including catecholaminergic polymorphic ventricular tachycardia (CPVT), arrhythmogenic right ventricular cardiomyopathy (ARVC), idiopathic ventricular fibrillation (I-VF) and atrial fibrillation (AF). In this study, we aimed to characterize Ca2+ release properties of RyR2s carrying the above 4 types of disease mutations. Wild type and mutant RyR2 channels were expressed in HEK293 cells and spontaneous Ca2+ oscillations were monitored by live-cell Ca2+ imaging using Ca2+ indicators for cytoplasm (fluo-4, GECOs) and ER (CEPIAs). In addition, the Ca2+-induced Ca2+ release (CICR) activity were determined with [3H]ryanodine binding assay. There were good correlations between CICR activity, Ca2+ oscillation frequencies and ER Ca2+ levels among all of mutants examined. While all CPVT mutants showed enhanced CICR activity, I-VF mutants showed divergent CICR profiles. Our results suggest that further analyses of experimental results and clinical data are needed to understand mechanisms of arrhythmogenic diseases due to RyR2 mutations.