Notably, the coordinated reduction in Arg-1+ populations (shared by N2 neutrophils and M2 macrophages) suggests chitosan disrupts immunosuppressive arginase-mediated pathways, while the TNF-α/MHCII axis likely enhances antigen presentation and cytotoxic immune cell recruitment, mechanistically linking myeloid cell reprogramming to the observed tumor suppression. The gene discussed is TNF; the disease is neoplasm.