In congruence with these reports, we previously found that Calsarcin-1 knockout mice do not exhibit cardiac hypertrophy phenotype at baseline in mixed genetic background notwithstanding striking upregulation of fetal genes and contractile dysfunction; however, these mice displayed strict DCM phenotype, devoid of hypertrophy, even when back-crossed for more than 10 generations to obtain the desired mutation in pure C57BL/6 background. This evidence concerns the gene MYOZ2 and familial dilated cardiomyopathy.