This work has shown that the mutation of CIC in glioma was mutually exclusive to MAPK genomic driver alterations, specifically NF1, BRAF, and KRAS. Further, characterization of MAPK activation via MPAS revealed higher activation for mutated CIC in comparison to wild-type CIC. This observation is in line with other studies that discuss the negative correlation between unaltered CIC, MAPK activation, and MAPK driver expression [8, 13, 14, 26]. Here, KRAS is linked to glioma.