Those with higher frequency of somatic mutations and tumor-specific neoantigens corresponded to double-strand break repair and mismatch repair subtypes, which were found to have higher expression of antitumor immunity, including activation of CD8+ T lymphocytes and overexpression of regulatory molecules (CTLA-4, PD-1, and indolamine 2,3-dioxygenase 1 [IDO1]) [47]. Here, PDCD1 is linked to neoplasm.