HRAS and colorectal carcinoma: To validate our hypothesis, we first analyzed a public cohort of 151 CRC cell lines with gene expression and cetuximab sensitivity data (GSE59857).45 To avoid any potential confounding factors, we focused on 28 microsatellite stable cell lines without KRAS, NRAS, HRAS, BRAF, and PIK3CA mutations, which have been shown to be significantly associated with refractory cetuximab response.46 Using the established scoring formula for CRC, we calculated risk scores followed by stratification of all cell lines into low-, intermediate-, and high-risk groups.