This was perhaps also to be expected, because life-long loss of KCa3.1 in complete KCa3.1-KO [24] does not show an overt phenotype at the intestinal level or epithelial level but shows endothelial dysfunction [25], defects in erythrocyte volume regulation and adaptive and slowly progressing splenomegaly [24], behavioral alterations [26] and the development of less experimental fibrosis [9], brain damage post experimental mean cerebral artery occlusion [27], and tracheal transplant obstruction [13]. The gene discussed is KCNN4; the disease is Splenomegaly.