We again found that complete deletion of Bmal1 required that the AVP-ires-Cre mice be in the homozygous state (i.e., AVPcre/cre); unfortunately, this also produced profound diabetes insipidus in these mice, likely secondary to disruption of AVP function (allele itself or Bmal1) in the supraoptic hypothalamus. This evidence concerns the gene BMAL1 and Central diabetes insipidus.