The contributions of many of these inflammatory signaling activators (TLRs, MYD88, TRIF, IL1R1, IRAK1/4, TRAF6, and NF-κB) and suppressors (IRAK3, TOLLIP, SOCS1, RNF216, IL1RL1, IL36RN, and TNFAIP3) in PCa remain poorly studied, despite the increasing association in the scientific literature of chronic inflammation with PCa initiation, progression, immunosuppression, and therapy resistance [301]. This evidence concerns the gene SOCS1 and posterior cortical atrophy.