KCNN4 and sickle cell disease: Secondly, sickle cell disease patients have increased expression of the NMDA-receptor on their RBC membranes, causing pathological influx of Ca2+ after stimulation with receptor agonists (such as glycine and homocysteic acid) (Hänggi et al., 2014) which could contribute to dehydration mediated by KCNN4.