These PRKCA variants are scattered throughout the gene without clustering in the kinase or other functional domain and are predominantly from cancer types with conspicuously high somatic mutational burden such as melanoma and microsatellite unstable gastrointestinal carcinoma (Supplementary Figure 6), suggesting that a majority of these PRKCA variants in tumors other than chordoid gliomas are likely to be passenger or bystander mutations. This evidence concerns the gene PRKCA and digestive system carcinoma.