Guided by above considerations, correlations between high expression of COX2 in human BlCa tissues and tumor progression and treatment resistance [35,36,37,38,39,40,41], the ability of COX2 blocker, celecoxib, to counteract tumor growth in BlCa-bearing animals (either receiving BCG or not) [15,41,42,43] and our observations that CCL22, CXCL12, and CXCL8 are induced as an undesirable side effect of BCG in BlCa tissues [7], we evaluated the role of PGE2 and its mechanistic basis in the regulation of baseline and BCG-induced inflammation in human BlCa TME. This evidence concerns the gene CXCL12 and bladder transitional cell carcinoma.