The fetal EH-myomesin alternatively spliced form of "MYOM1" has been shown to be reexpressed at an early timepoint in the progression of dilated cardiomyopathy, coincident with isoform switches in titin. "MYOM1" has also been shown to be abnormally spliced in patients with myotonic dystrophy type I; specifically, exon 17a. Skelemin/Myomesin-1 has been shown to interact with: