In addition to flow-mediated HLHS (extrinsic factors), intrinsic factors such as apoptosis may contribute to the development of HLHS.10 The prolonged administration of human induced pluripotent stem cells from patients with HLHS advocated intrinsic cardiomyocyte disorders.4 Furthermore, genetic or environmental interruption of the Ca2+ signalling pathway and mutations in Rbfox2 may disturb cardiac chambers, outflow tracts, and valves.6,9. This evidence concerns the gene RBFOX2 and hypoplastic left heart syndrome.