KRAS mutations are very frequently observed in human LADC, but the RAS tumor driver pathway is also activated in up to half of human LSCC tumors, most commonly due to transcriptional up-regulation and amplification of KRAS and the upstream receptor tyrosine kinases EGFR and FGFR1 (Fig. S1 A; Cancer Genome Atlas Research Network, 2012; Campbell et al., 2016). The gene discussed is EGFR; the disease is neoplasm.