The results revealed that CM Tln2 was indispensable for appropriate β1D-integrin expression and that presumably Tln1 could take the place of Tln2 in preserving heart function, however, that lack of both Tln forms from the heart-muscle cell resulted in myocyte instability and a dilated cardiomyopathy. The gene discussed is TLN2; the disease is dilated cardiomyopathy.