SCN4B encodes the β4 subunit of voltage-gated sodium channels (Nav), serving as a regulatory component that modulates channel activity and localization in excitable membranes 1. The protein functions as an auxiliary subunit that participates in the functional modulation of Nav channels, contributing to membrane depolarization and electrical signal propagation 1. Beyond its classical role in excitable tissues, SCN4B has emerged as a metastasis-suppressor gene in cancer biology. In breast cancer, reduced SCN4B expression correlates with high-grade tumors and promotes cell migration through RhoA pathway activation, independent of its sodium channel function 2. Similarly, SCN4B is downregulated in lung adenocarcinoma, where higher expression associates with better prognosis and inhibits tumor progression by suppressing the cGMP-PKG signaling pathway 3. Regarding cardiac disease associations, SCN4B was initially reported to cause Long QT syndrome; however, recent evidence-based reappraisal classified it as having only limited or disputed evidence for LQTS causation 4. In neurological contexts, SCN4B knockout mice demonstrate increased sensitivity to sedative effects of ethanol and other drugs, though without affecting ethanol consumption behaviors 5. These findings highlight SCN4B's dual roles in both ion channel regulation and cancer suppression.