KCNK1 is a potassium two pore domain channel that contributes to membrane potential regulation and ion transport across multiple tissues. The channel forms dimers with low intrinsic activity as homodimers but exhibits enhanced function when heterodimerizing with other KCNK family members 1. In the nervous system, KCNK1 plays a critical role in neuropathic pain regulation, where its downregulation in dorsal spinal horn neurons contributes to pain hypersensitivity through a ciRNA-Kat6b/miRNA-26a/Kcnk1 pathway 2. KCNK1 has also been implicated in trigeminal neuralgia, with genetic variants potentially contributing to disease susceptibility 3. In cardiac tissue, KCNK1 expression differs between atrium and ventricle, and its downregulation is associated with arrhythmic sudden cardiac death, suggesting involvement in lethal arrhythmia susceptibility 4. Emerging evidence indicates KCNK1 has significant oncological relevance, being overexpressed in both breast and bladder cancers where it promotes tumor proliferation, invasion, and metastasis 567. In breast cancer, KCNK1 activates lactate dehydrogenase A and increases glycolysis, while its knockdown enhances chemotherapy sensitivity 7. These diverse functions position KCNK1 as both a potential therapeutic target and prognostic biomarker across multiple disease contexts.