Several TA proteins have been linked to cardiomyopathy (including dysferlin, emerin, junctophilin-2, phospholamban, nesprin-1, and nesprin-2), and failure to correctly localize one or more of these proteins, due to defective ASNA1-mediated membrane insertion, may be responsible for the cardiac phenotype observed in both patients and zebrafish. This evidence concerns the gene EMD and cardiomyopathy.