PDPN is part of the co-inhibitory gene module upregulated in cancer, and PDPN deficiency in T cells results in retardation of tumor growth.123 The protein C receptor (PROCR) is another molecule highly expressed in Th17 cells and exhausted T cells.123,245 In autoimmunity, PROCR was found to act as a negative regulator of Th17 pathogenicity.245 PROCR regulated the pathogenic gene module of Th17 cells by modulating expression of IL-1R, a major driver of pathogenic Th17 cells, and T cell-specific deficiency of PROCR resulted in exacerbated EAE. This evidence concerns the gene PDPN and neoplasm.