LTBP4 and cardiomyopathy: Using the γ-sarcoglycan- (Sgcg-) null mouse model of muscular dystrophy and cardiomyopathy on a DBA2/J background, a polymorphism in the coding region of the latent TGF-β-binding protein 4 gene (Ltbp4) resulting in a 12-amino-acid deletion in LTBP4 protein was found to be responsible for increased proteolysis, fibrosis, and atrophy in these mice [44].