In the tumor setting, PROCR deficiency inhibited tumor growth with decreased frequencies in exhausted (TIM-3High and PD-1High) CD8+ T cells.123 Another example is the glycosphingolipid receptor GPR65 that was identified in vivo to co-vary with pro-inflammatory genes in single-cell RNA-sequencing of Th17 cells during EAE.53 Interestingly in contrast to PDPN and PROCR, GPR65 was validated as pathogenic driver of Th17 cells in EAE. The gene discussed is PROCR; the disease is neoplasm.