EIF3B (eukaryotic translation initiation factor 3 subunit B) is a core component of the eukaryotic translation initiation complex with multifaceted roles in gene expression and disease pathogenesis. Mechanistically, EIF3B functions as a translation initiation facilitator by directly interacting with other initiation factors and ribosomal RNA to promote the assembly of translation-initiation complexes 1. In viral infections, EIF3B participates in ribosomal termination-reinitiation events [PMID:18056426, per UniProt]. Additionally, EIF3B localizes to cytoplasmic condensates containing insulin mRNA in pancreatic β-cells, where it regulates glucose-stimulated insulin translation 2. EIF3B exhibits significant disease relevance across multiple cancer types. In hepatocellular carcinoma, YTHDF2 recruits EIF3B to facilitate ETV5 translation, driving immune evasion and angiogenesis 3. In prostate cancer bone metastasis, PUS1 stabilizes EIF3B protein, promoting metastatic progression; notably, targeting PUS1 suppresses metastasis through EIF3B degradation 4. In KRAS-mutant colorectal adenocarcinoma, EIF3B promotes cancer progression by regulating TBK1 and PI3K/AKT signaling pathways 5. Conversely, EIF3B knockdown inhibits ovarian cancer cell proliferation and increases apoptosis 6. In ischemic stroke, TIPARP-mediated EIF3B interaction causes mitochondrial dysfunction; inhibiting this interaction rescues brain injury 7. EIF3B is identified as a shared therapeutic target in rheumatoid arthritis and osteoarthritis 8, suggesting its broad pathophysiological significance.