PTGS2 and neoplasm: Emerging evidence suggests alterations in the primary BA pool as a crucial pathogenetic moment contributing to hepatic carcinogenesis through the disruption of various signaling pathways [including Janus Kinase-Signal Transducer and Activator of Transcription (JAK-STAT3), cyclooxygenase-2 (COX-2), and NF-kB], amplifying the polarization of M2-like tumor-associated macrophages (TAM-M2), and enhancing the local production of inflammatory mediators [IL-6, IL-1beta, and TNF-alpha] via activating inflammasome [76,77].