Kcne3, also known as MiRP2, is a gene encoding a single transmembrane-spanning ion channel regulatory subunit. It primarily functions to regulate voltage-gated potassium (Kv) channels, especially in co-assembly with the KCNQ1 Kv α subunit. In the intestine, constitutively active KCNQ1-KCNE3 channels are important for potassium and chloride secretion. Kcne3-related research helps understand the regulation of potassium channels and related physiological processes [1,2,4,6].

In Kcne3-/-mice, the deletion led to arrhythmogenesis through a novel mechanism. There was secondary hyperaldosteronism associated with adrenal-specific lymphocyte infiltration, which impaired ventricular repolarization. Kcne3 deletion also impaired skeletal muscle function, increasing oxidative metabolic gene expression, altering muscle fiber type, and affecting muscle contractile force and ion currents in myoblasts [3,5].

In conclusion, Kcne3 plays a crucial role in regulating potassium channels, which is essential for physiological functions in the intestine, heart, and skeletal muscle. The study of Kcne3 knockout mouse models has revealed its significant role in arrhythmogenesis and skeletal muscle function, providing insights into related disease mechanisms [3,5].