Hair Development, Growth, and Loss 46 in skin can be explained by a reaction-diffusion (R-D) model. The R-D model was first proposed by Turing, in which small spatial fluctuations of an activator and inhibitor could lead to the establishment of a spatial pattern of morphogens.20,21 Sick et al. investigated the functions of Wnts and Dkks as activator and inhibitor in the regulation hair follicle patterning in developing murine skin.22 Both Wnts and Dkks are secreted into the extracellular space and can therefore participate in such R-D interactions. Given the key role of Wnt protein in hair follicle fate induction, its activity within and around the developing hair placode must be tightly controlled. Expression of the protein Dkk1, which inhibits Wnt, is actually controlled by Wnts. Because of its smaller size, Dkk1 could easily diffuse farther into the epidermis, thereby inhibiting Wnt signaling in the interfollicular epidermis, while the larger Wnt molecules would remain within the site of placode for further development. Thus, moderate overexpression of the hair follicle activator Wnt would increase hair follicle density, while moderate overexpression of hair follicle inhibitor Dkk1 would decrease hair follicle density. Not every ectodermal progenitor cell23 will adopt a follicular fate. This implies that there must be a mechanism, which either promotes or inhibits hair follicle fate. The key determinants in the development are a set of reciprocal signaling molecules traveling between epithelial cells of the surface ectoderm and underlying dermal fibroblasts.23 Members of several families of secreted signaling molecules are expressed in the developing hair follicles and mediate reciprocal communication, including the Wnt/wingless family, the hedgehog family, bone morphogenetic protein (Bmp), fibroblast growth factor (Fgf), and tumor necrosis factor (TNF).23 Different combinations of these signals may dictate whether a hair follicle or interfollicular epidermis will develop. Wnt, Ectodysplasin A1 (Eda-A1) and Noggin are confirmed hair placode-inducing signals.24 It has been demonstrated that Wnt/β-catenin and Eda/ Edar/NF-ĸB signaling pathways are indispensable in initiation and