Collinsella contributes to the pathogenesis in rheumatoid arthritis by increasing gut permeability, reducing the expression of tight junction proteins in epithelial cells, and inducing the expression of IL-17 cytokines (Chen et al., 2016), which may result in the pathologic effects by recruitment of neutrophils and activation of NF-kB signaling (Derrien et al., 2009). The gene discussed is NFKB1; the disease is rheumatoid arthritis.