Genome-wide methods, such as GWAS and expression studies, have linked a variety of NFκB-associated pathways to prostate cancer progression, including inflammatory processes (CXCL12, IL4, IL6, IL6ST, PTGS2, STAT3, and TNF) [13], cellular differentiation (LEPR, CRY1, RNASEL, IL4, and ARVCF) [14], and cell cycle regulation (FoxM1, SPP1) [15]. This evidence concerns the gene STAT3 and prostate cancer.