Identification of positive correlation between tumor specific FAP+ fibroblasts and SPP1+ macrophagesPossible regulation of the interaction between FAP+ fibroblasts and SPP1+ macrophages via chemerin, TGF-β, and interleukin-1, and stimulation of the formation of immune-excluded desmoplastic structure and limitation of T cell infiltrationIdentification of patients with high FAP or SPP1 expression achieved less therapeutic benefit from an anti-PD-L1 therapy cohortPotential therapeutic strategy via disrupting FAP+ fibroblasts and SPP1+ macrophages interaction to improve immunotherapy. The gene discussed is SPP1; the disease is neoplasm.