In fact, hiPSC-CMs harboring a mutation truncating the sarcomere protein titin (TTN), a known common cause of DCM, did not show any abnormal contractile function and were comparable with wild-type hiPSC-CMs in a 2D culture platform but exhibited significantly reduced contractility and decreased sarcomere length when fabricated in 3D constructs of self-assembling cardiac microtissues that worked against the elastic resistance between two PDMS pillars [200]. Here, TTN is linked to familial dilated cardiomyopathy.