Hair Development, Growth, and Loss 52 by Fgf5-deficient mice, which have a prolonged anagen phase resulting in an angora hair phenotype.50 Again, in humans, hair cycling is generally divided into the three phases of anagen, catagen, and telogen. The duration and proportion of each phase is different depending on the locations on the body. On the scalp, the average duration of anagen, catagen, and telogen is three years, three weeks, and three months, respectively. Anagen accounts for 90% of scalp hair, telogen 10% and catagen less than 1%. The balanced propagation of hair cycle is important changes in the duration or proportion of each hair cycle stage will lead to hair disorders.38 Hair Follicle Stem Cells As a self-regenerating mini-organ, the hair follicle and its connective tissue sheath are an abundant source of epithelial, melanocyte, and mesenchymal stem cells. Taking advantage of their slow cycling properties, label-retaining experiments have identified adult follicular stem cells in the hair follicle bulge region of mice and humans.40 This led to the “bulge activation hypothesis,” which states that, at the onset of anagen, a subset of hair follicle stem cells is activated and starts to divide. Their daughter cells migrate to the base of the follicle where they start to proliferate, and normally are named as transiently activated matrix cells because they only divide a few times before differentiation. In vivo labeling and grafting studies confirm the ability of bulge stem cells to give rise to all cell lineages of the mature hair follicle.51 It has also been demonstrated that they possess the ability to generate not only hair follicles, but also sebaceous glands and interfollicular epidermis. Keratin 15 (K15) and CD34 are typically used as markers for murine epithelial stem cells in the hair follicle, and K15 has also been used to isolate putative murine bulge stem cells.52-54 Genes typically up-regulated in the bulge include stem cell markers such as c-kit ligand, ephrin tyrosine kinase receptors, CD34, and transcription factors Barx2, Sox9, Lhx2, and Tcf3. As expected, down-regulated genes include proliferation-associated proteins such as Ki67 and Cdc25C.55, 56