Remarkably, however, we observed a strong bias among expanded insertions for signaling pathways, for example, downstream components of receptor tyrosine kinases signaling (Braf, Gab1, Nf1, Pten, Sos1), in agreement with data from human tumor studies that alterations in cellular signaling pathways are main drivers of tumorigenesis [14]. The gene discussed is SOS1; the disease is neoplasm.