We also recently mutated Thbs4 so that it was not secreted or processed through the sarcolemma, which specifically inhibited membrane residence of β-dystroglycan, β-sarcoglycan, and δ-sarcoglycan from the dystrophin-glycoprotein attachment complex, promoting membrane instability and cardiomyopathy in mice20. This evidence concerns the gene ART4 and cardiomyopathy.