We have assessed the expression of MyBP-C isoforms, the structure of the skeletal muscles, and the functional characteristics of slow (soleus) and fast (extensor digitorum longus, EDL) skeletal muscles in the cMyBP-C null mouse model (t/t) ) [21] to test whether i) cMyBP-C is necessary for normal adult skeletal muscle structure, ii) DCM-induced myopathy leads to alteration in MyBPC expression, and iii) transcomplementation of skeletal MyBP-C isoforms compensates for the absence of cMyBP-C in the heart, compared to the wild-type (WT) control mice. The gene discussed is MYBPC2; the disease is myopathy.