The main results are (1) successful genetic engineering of two hiPSC lines, a homozygous OCTN2 (N32S) mimicking the patient situation and an OCTN2 (–/–) knockout, (2) replication of the PCD DCM phenotype involving low acylcarnitine tissue content and force, complex metabolic remodeling, and ultrastructural alteration, (3) corroboration of the of OCTN2 (N32S) phenotype by high-level concordance with OCTN2 (−/−) across various assays, (4) discovery of ferroptosis linked to fibroblast activation as a novel PCD DCM mechanism. The gene discussed is SLC22A5; the disease is familial dilated cardiomyopathy.