In addition, we verified by exomeanalysis that the patient did not have any pathogenic variants in the genes associatedwith Noonan Syndrome and other rasopathies (PTPN11,SHOC2, KRAS, CBL,SOS1, RAF1, HRAS,NRAS, RASA1, SPRED1,BRAF, MAP2K1, MAP2K2, RIT1 andRRAS) (Rauen, 2013; Ekvall et al., 2015). This evidence concerns the gene KRAS and Noonan syndrome.