NCFCs display significant genetic and phenotypic heterogeneity: on the one hand, mutations in the same gene may be responsible for different syndromes, as is the case for Noonan syndrome and LS, mostly caused by mutations in the PTPN11 gene; on the other hand, dysfunction of different proteins at various levels of the RAS/MAPK cascade can lead to similar clinical presentations [7,8]. This evidence concerns the gene PTPN11 and Noonan syndrome.