Several studies have postulated possible molecular mechanisms by which dilated cardiomyopathy results from the deletion of Bmal1, including increased expression of collagen (I and III) and MMP 9, 13, and 14 [116], increased expression of molecular marker for hypertrophy (Mcip1) [119], and altered circadian oscillation of a number of genes associated with myosin heavy chain [120], cardiac metabolism, and the insulin signaling cascade [120]. This evidence concerns the gene BMAL1 and dilated cardiomyopathy.