However, the β1-Integrin/Ilk complex is necessary for normal cardiac development and contractile activity, and inhibition within cardiomyocytes and PCs beyond a certain threshold results in cardioblast adhesion defects and arrhythmia in Drosophila [141], while β1-Integrin/Ilk knock-out mice develop myocardial fibrosis, cardiomyopathy, and heart failure [143,225]. This evidence concerns the gene ILK and heart failure.