Through a proteome analysis, they showed that granulocyte macrophage colony-stimulating factor (GM-CSF) can contribute to the pathogenesis of RA by upregulating LCN2 in neutrophils, followed by the induction of a series of enzymes, such as cathepsin D, transitional endoplasmic reticulum ATPase (TERA), and transglutaminase 2 (tg2) in synoviocytes, which could contribute to the proliferation of synovial cells and infiltration of inflammatory cells inside the synovium [166]. Here, LCN2 is linked to rheumatoid arthritis.