IL-17 signaling has been shown to promote carcinogenesis. Further, studies have shown that inhibiting signaling from this cytokine slows down oncogenesis initiation, suggesting that IL-17 inhibition may be used to halt the early stages of tumor growth. Importantly, studies utilizing mouse models have found that increased IL-17 levels were correlated with high PD-L1 expression. Further, combining IL-17 and a PD-1 blockade induced higher levels of cytotoxic T cells and tumor regression [48]. This evidence concerns the gene CD274 and neoplasm.