Although Slc5a5, Slc26a4, and Slc26a7 have been identified as iodide transporters and genetic abnormalities in these genes are known to cause CH in humans, phenotypic analysis of deficient mice suggests that the effect of Slc26a4 on the mouse thyroid is less prominent than that of Slc5a5 and Slc26a7 under normal conditions. Here, SLC26A7 is linked to cyclic hematopoiesis.