In present study, after more than 10 back-crosses to obtain Calsarcin-1 null mouse in pure C57BL/6 background in order to study the effect of genetic background, if any, mice displayed dilated cardiomyopathy phenotype with contractile dysfunction and increased expression of fetal genes nppa, and nppb in addition to upregulated rcan1-4 without any signs of hypertrophy. This evidence concerns the gene MYOZ2 and dilated cardiomyopathy.