As expected, VdrΔAF2 mice do not develop alopecia, as only mutations resulting in DNA binding defects, RXR dimerization defects, or complete absence of VDR cause these disturbances in hair cycling.10,25–27 Here, we show that the effects of coactivator-independent VDR signaling extend beyond those observed in hair follicle homeostasis,14,28 evidenced by the more severely impaired mineral homeostasis and bone phenotype observed in VdrΔAF2 mice compared to Vdr−/− mice. Here, VDR is linked to alopecia.