Furthermore, two additional rickets models derived from Hyp mice (Figure 8) and targeted stabilization of β-catenin in Ocys (Figure 9) showed a very similar osteomalacia phenotype due to a sharp increase in β-catenin in Ocys (i.e., the causative factor for the onset of rickets); this event led to an increase in Ob-like cell numbers and activities but a decrease in mature Ocy numbers and their activities. Here, LEP is linked to rickets.