Three pathogenic RASopathy variants (PTPN11, SOS1) were consistent with Noonan syndrome, an autosomal dominant syndrome of craniofacial and cardiac anomalies often accompanied by prenatal nuchal edema, chylothorax, and hydrops, as well as postnatal lymphedema, GLA, and chylothorax.1,17,36,40 The last likely pathogenic RASopathy variant was a frameshift truncation variant in RASA1. The gene discussed is SOS1; the disease is Noonan syndrome.