Autoinflammation occurring through activation of the inflammasome has also been proposed as an driver of IBD,14 with G6PC3-deficient neutrophils producing significantly increased levels of pro-inflammatory cytokines in response to lipopolysaccharide.14 As rates of apoptosis in G6PC3-deficient neutrophils are consistently enhanced upon TNF-α stimulation,27 pro-inflammatory states may perpetuate neutropenia. The gene discussed is TNF; the disease is inflammatory bowel disease.