Four of the 11 selected proteins participated in interactions with candidates known to participate in NF-κB activation, including (i) IκBκE; which activates NF-κB via TRAF-2 [35], (ii) TRAF-6; an NF-κB regulator that plays a critical role in human autoimmune diseases including arthritis [36], (iii) TNF-receptor superfamily member TNFRSF21; which activates NF-κB and MAPK8 pathways [37,38], and (iv) mitogen-activated protein kinase kinase kinase-14 (MAP3K14), also called the NF-kappa-beta-inducing kinase (NIK); which activates NF-κB via TRAF-2 [39]. This evidence concerns the gene TRAF6 and arthritic joint disease.