In the present study, we set out to explore global proteomic features of BRAFV600E mutant colon cancer cells in comparison with KRAS mutant/BRAF wild-type and double wild-type KRAS/BRAF colon cancer cells in order to identify novel druggable vulnerabilities of BRAF-mutated colon cancer that could play a role in regulating the cell response and resistance to BRAFV600E inhibition by vemurafenib. Here, KRAS is linked to colonic neoplasm.