Based on our data above and the findings that inflammation can drive the development of CRC, that oncogenic KRAS is known to induce an inflammatory environment in the colon, and that chemotherapies also cause increased inflammation in the colon, we hypothesized that intrinsic or chemotherapy-induced inflammation may result in a tumor microenvironment that renders cells resistant to trametinib [22–24]. The gene discussed is KRAS; the disease is neoplasm.