In the later stages of sepsis, macrophages polarized toward the M2 phenotype actively promote Treg expansion and functional activity through multiple mechanisms, including the secretion of TGF-β and IL-10, expression of PD-L1, and arginine depletion mediated by Arg1, thereby collectively contributing to the establishment of immune paralysis [50,62,63]. The gene discussed is ARG1; the disease is Sepsis.