VDR and cancer: β‐catenin acts as a transcription factor with VDR to enable proliferation but also acts, as a component of the membrane E‐cadherin–catenin complex, to facilitate differentiation.(51) Deletion of VDR and/or CaSR in epidermal keratinocytes of mice disrupts epidermal differentiation, impairs wound healing,(52) and predisposes to cancer.(53) 1,25(OH)2D also promotes the innate immune function of keratinocytes by inducing the Toll‐like receptor 2 (TLR2) and its co‐receptor CD14.