With the increasing knowledge on RA pathophysiology and genomewide studies demonstrating that loci related with TNF signaling pathways such as the NF-kB signaling pathway (TRAF1/C5, TNFAIP3, and REL) and other pathological processes such as enhanced citrullination (PADI4) may increase RA risk, it is compelling to explore how those loci could also influence the anti-TNF response [21–28]. Here, NFKB1 is linked to rheumatoid arthritis.