Along those lines, our laboratory, using CaMKIIγ/CaMKIIδ double knockout (DKO) mice, showed that pathological and physiological cardiac hypertrophy in mice was not primarily CaMKII dependent, but rather attributable to the calcineurin (CnA)–NFAT axis, while CaMKII was responsible for maladaptive effects, i.e., systolic and diastolic dysfunction [44]. This evidence concerns the gene CAMK2G and cardiac hypertrophy.