What is more, ILK acts as a mechanosensory element in the human heart, mediating cardiomyocyte force transduction through regulation of the vital calcium regulatory protein sarcoplasmic/endoplasmic reticulum Ca2+ATPase isoform 2a (SERCA-2a) and phosphorylation of phospholamban (PLN), which provides additional support for the link of ILK with DCM and highlights its potential role as the therapeutic target [20]. This evidence concerns the gene PLN and familial dilated cardiomyopathy.