Moreover, in early RA patients, antiapoptotic cytokines (e.g., IL-4, GM-CSF, and G-CSF) that are found in their SF may lead to defects and low levels of apoptotic death in neutrophils, suggesting that their engulfment by macrophages after secondary necrosis elicits a proinflammatory response. This evidence concerns the gene IL4 and rheumatoid arthritis.