CDYL repressed Kv2.1 transcription by promoting histone 3 lysine 27 trimethylation (H3K27me3) at the Kcnb1 intron region and knockdown of Kv2.1 reversed the pain‐related phenotypes of Cdyl deficiency mice. Here, KCNB1 is linked to hyperinsulinemic hypoglycemia, familial, 4.