Against this background, Carvajal-Vergara and colleagues generated hiPSCs from two patients with the heterozygous T468M mutation in the PTPN11 gene and highlighted important molecular mechanisms in the signaling pathways responsible for the cardiac hypertrophic phenotype in LEOPARD syndrome, such as the increased phosphorylation of specific proteins such as MEK1 in LEOPARD-hiPSC-CMs compared to wild-type, demonstrating that RAS-MAPK signaling is perturbed in LEOPARD syndrome [140]. This evidence concerns the gene MAP2K1 and Noonan syndrome with multiple lentigines.