Through a proteomic approach, GM-CSF was found to induce LNC2 upregulation in neutrophils, which in turn can influence synoviocyte behavior through the release of several enzymes, such as transglutaminase 2 (TG2), cathepsin D, and transitional endoplasmic reticulum ATPase (TERA) (Figure 1), which contribute to both inflammation of synovium and proliferation of synovial cells, promoting the RA state [137]. The gene discussed is VCP; the disease is rheumatoid arthritis.