Study of [37] some of the published mutations [(R131W [35] and R141W [36] in exon 10), and (Lys 210 del [34,35], R205L [35] in exon 13)], in the amino-terminal tail of TNNT2 gene reported to be responsible for dilated cardiomyopathy (DCM); along with other 4 thin filaments mutations, reconstituted with a 1∶1 ratio of mutant∶wild type proteins, all showed reduced Ca2+ sensitivity of activation in ATPase and motility assays, and all showed lower maximum Ca2+ activation. The gene discussed is TNNT2; the disease is familial dilated cardiomyopathy.