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Our findings suggest that FABP4-mediated macrophages may promote proliferation and migration phenotypes in NB cells through deactivating NF-κB-IL1α pathway by ubiquitinating ATPB. This study reveals the pathologic and biologic role of FABP4-mediated macrophages in NB development and exhibits a novel application of targeting FABP4 in macrophages for NB treatment. Fibroblast-like synoviocytes (FLS) and articular chondrocytes (AC) derive from a common pool of embryonic precursor cells. They are currently believed to engage in largely distin
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