Here, RNA sequencing and functional analyses were combined with cardiac engineered microtissues from healthy, mutated, and isogenic hPSC lines to demonstrate that truncations in the A-band domain of TTN cause DCM, whereas truncations in the I band are better tolerated, because alternative splicing excludes I-band exons from most mature TTN transcripts [156]. This evidence concerns the gene TTN and familial dilated cardiomyopathy.