There was also a high extent of coassociation of A59T with alterations in ARID1A, a regulator of transcription implicated in chromatin remodeling that includes a DNA-binding domain which binds AT-rich sections of DNA; colorectal tumors with mutant ARID1A are characterized by higher rates of MSI-H and/or TMB-high status and T-cell infiltration [9]. This evidence concerns the gene ARID1A and colorectal neoplasm.