In addition, OV infection can directly upregulate MHC-I expression on tumor cells (19, 20), or indirectly enhance antigen presentation by activating the cGAS–STING pathway and promoting type I interferon production, which further increases the expression of co-stimulatory molecules (CD80, CD86) and MHC-I/MHC-II molecules on DCs (25–28), thereby helping overcome the impaired antigen presentation frequently observed in osteosarcoma (19, 20). This evidence concerns the gene CGAS and neoplasm.