KCNN4 and Fabry disease: In the present study, we provided additional evidence for such defective KCa3.1-regulation in FD fibroblasts and also in NPC fibroblasts from a male patient, which seemed predominantly to rely on impaired de novo-KCa3.1 gene expression, thus similar to that was found in earlier studies (Choi et al., 2015; Choi and Park, 2016).