KCNMB1 encodes the β1 regulatory subunit of large-conductance calcium-activated potassium (BK) channels, which modulates the gating kinetics and calcium sensitivity of the KCNMA1 pore-forming subunit. This regulatory function enables negative feedback control of smooth muscle contraction by enhancing calcium sensitivity and slowing channel activation/deactivation kinetics. Clinically, KCNMB1 dysregulation is implicated in multiple pathologies. The KCNMB1 E65K polymorphism is associated with essential hypertension risk in Asian populations 1. In cardiovascular disease, reduced KCNMB1 expression drives vascular smooth muscle cell phenotypic switching from contractile to proliferative states, ultimately promoting apoptosis 2. Conversely, KCNMB1 upregulation occurs in idiopathic pulmonary fibrosis, where increased BK channel activity promotes myofibroblast differentiation through calcium-dependent mechanisms 3. KCNMB1 expression is hypoxia-inducible via HIF-1α transcriptional regulation 4, and atherogenic factors like 7-ketocholesterol suppress KCNMB1 through aryl hydrocarbon receptor signaling, contributing to vascular rigidity 5. Additionally, KCNMB1 upregulation occurs in high-grade glioblastomas and promotes tumor cell proliferation and migration 6. KCNMB1 also regulates cerebral artery responses to ethanol via BK channel modulation 7. These findings suggest KCNMB1 represents a therapeutic target across cardiovascular, pulmonary, and neoplastic diseases.