We believe that the association heredescribed of 1p13.2 microdeletion involving hemizygosity for NRAS andclinical features of Noonan syndrome, represent a further example of the model proposedby Nowaczyk et al. (2014),according to which, haploinsufficiency of a gene in the Ras/MAPK pathway may causedysregulation of the pathway and produce a RASopathy phenotype. The gene discussed is NRAS; the disease is Noonan syndrome.