In this regard, a significant number of gain-of-function SOS1 mutations (and, more rarely, SOS2 mutations), resulting in subsequent hyperactivation of RAS signaling, have been identified in inherited RASopathies, such as Noonan syndrome (NS) or hereditary gingival fibromatosis, as well as in various sporadic human cancers, including endometrial tumors and lung adenocarcinoma, among others [5]. This evidence concerns the gene SOS1 and RASopathy.