Also, CMS3 tumor epithelial cells showed KRAS signaling was upregulated at the transcriptomic level in CMS3 which also demonstrated immunological and immune evasion signatures (JAK-STAT signaling), implying this subtype is not entirely immune deficient, consistent with the observation that a subset of MSI tumors are represented by this subtype [10]. Here, SOAT1 is linked to neoplasm.