INHBB (inhibin subunit beta B) encodes the beta-B subunit of inhibin B, a TGF-β superfamily member with context-dependent functions across multiple physiological systems. In reproduction, inhibin B (α/β-B dimer) suppresses follicle-stimulating hormone (FSH) secretion from the anterior pituitary by antagonizing activin signaling through type II activin receptors 1. INHBB variants that disrupt activin B biosynthesis can alter testis germ cell content, though fertility may remain intact in some cases 1. Beyond reproduction, INHBB is widely expressed in brain, liver, kidney, and adrenal tissues 2. In pathological contexts, INHBB plays complex roles. In renal fibrosis, tubule-derived INHBB activates interstitial fibroblasts via activin B/Smad signaling in a paracrine manner, with expression regulated by the Sox9 transcription factor 3. In glioblastoma, INHBB promotes tumor progression and stemness through EGFR/AKT/ERK pathway activation and predicts poor survival 4. INHBB also functions as a senescence-associated secretory phenotype factor in diabetic pancreatic cancer, where INHBB receptor inhibition with bimagrumab demonstrates therapeutic efficacy 5. In recurrent implantation failure, reduced endometrial INHBB impairs decidualization via suppression of ADCY1-mediated cAMP signaling 6. Notably, INHBB shows potential pro-remyelinating properties in multiple sclerosis 7.