In normal skin, proliferating cells were detected in either the basal layer of epidermis or in germinative hair follicle bulbs at the base (Figure 4B). In the mutant skin, either BrdU incorporation or Ki67 expression was observed not only in cells in bulbs at the base of the hair follicle but also in bulb-like structures that were budding out from the ORS of the existing hair follicles (Figure 4G and 4G′). Each budding tip was becoming like a hair follicle bulb containing proliferating cells. Hence, despite the abnormal histology in the mutant skin, proliferation seems to be confined to bulb-like structures as in the normal skin (Figure 4G and 4G′). The exact locations of hair follicle bulbs were not as easy to define for some mutant follicles due to their disorganized structures. Interestingly, in the mutant skin, in addition to diffuse membrane-bound localization as in the normal skin, cells with strong cytosolic β-catenin localization were also observed frequently (Figure 4H and 4H′). These elevated β-catenin–expressing cells were usually surrounded by proliferating cells, forming bulb-like structures. Comparison of immunochemically stained serial sections showed that these intense cytosolic β-catenin stainings were usually found in either K14-positive K1-negative basal epidermis or K14-positive K6-negative basal ORS cells, and are surrounded by proliferating cells.