Moreover, G-MDSCs from Nlrp3-/- mice not only downregulated Lox1 and Pdl1 expression, which are associated with G-MDSC identity (34) and tumor immune evasion (35, 36), respectively, but also demonstrated enrichment in type I IFN signatures, which is linked to re-programming of granulocytic cells in the TME (32). The gene discussed is NLRP3; the disease is neoplasm.