The TNFRSF1A-GRN pair could directly bind to disturb the TNFα-TNFR interaction,29 while the C5AR1-RPS19 could promote tumor growth by facilitating the recruitment of tumor-infiltrating myeloid cells to tumors.30 In addition, the specific FN1-a4b7 and FN1-a4b1 receptor-ligand complexes indicated the existence of functional interactions between Mφ and all other immune cells (Fig. 3b and Supplementary Fig. 3e). The gene discussed is FN1; the disease is neoplasm.