These interconnected mechanisms act through several key molecular pathways involved in the pathogenesis of IBD, such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), Janus kinase 1 (JAK1), Signal transducer and activator of transcription 3 (STAT3), Toll-like receptor 4 (TLR4), mammalian target of rapamycin complex 1 (mTORC1), and interleukin signaling pathways including interleukin (IL)-17 and IL-23, all contributing to immune dysregulation, epithelial barrier disruption, and chronic intestinal inflammation [5]. This evidence concerns the gene TLR4 and gastroenteritis.