Studies have shown that MEK inhibition (MEKi) enhances the antitumor capacity of patients and can immunomodulate tumor cells and tumor‐infiltrating lymphocytes (TILs), and studies have utilized the CRISPR/Cas system‐mediated MEK1 KO to mimic tumor‐specific MEKi, and pharmacological MEKi using cobimetinib in colorectal cancer models, thereby distinguishing MEKi mediated and dependent mechanisms of immunomodulation. Here, MAP2K1 is linked to neoplasm.