Since, animal-based studies have recently indicated that Akt/PKB is critically regulated by ILK during cardiac function and dysfunction [8], [15], [16] and that Akt activation is dependent on the ILK/PINCH interaction [17], we hypothesized that the phosphorylation of Akt Ser 473 might also be elevated in DCM hearts. This evidence concerns the gene ILK and familial dilated cardiomyopathy.