The analysis has highlighted important roles of genes in infection related pathways in RA, including AKT3, ATF6B, ATP6V1F, ATP6V1G2, BAK1, CD28, CD40, CDK2, CSNK2B, FADD, FOXO1, HES5, HSPA1A, HSPA1B, HSPA1L, ICAM1, IL2, LAMA3, NOTCH4, PSMD3, STAT1, STAT4, TAB1, TAP1, TAP2, TAPBP, TNF, TYK2 and TNXB, suggesting that the elevated risk of infection in RA patients can be explained by the genetic inherence and pathobiology of the disease itself, independent of immunosuppressive treatment (Listing et al., 2013). This evidence concerns the gene FADD and rheumatoid arthritis.