While prior work identified isolated Fcγ receptor components in renal cancer (67), our network topology analysis reveals FCGR2A as the central hub coordinating myeloid cell reprogramming in obese microenvironments (34).Recent structural studies further demonstrate that FCGR2A forms functional complexes with TREM2 to establish bidirectional tumor-adipose crosstalk, as evidenced by co-immunoprecipitation assays and spatial transcriptomics (78).Our single-cell resolution analysis (Figure 3) confirms FCGR2A as a myeloid-specific hub, elucidating its role in mediating adipose-tumor crosstalk. Here, TREM2 is linked to neoplasm.