That NF-κB-associated TFs and NRF2 were inversely targeted was particularly interesting as there is evidence in the literature that these elements counter-regulate [26,27] and also that NRF2 protects against joint damage in the antibody-induced arthritis (AIA) model of RA by limiting oxidative stress-induced cartilage destruction [28]. The gene discussed is NFKB1; the disease is rheumatoid arthritis.