We further demonstrated that impaired HD formation in Scd1−/− keratinocytes accelerated their proliferation and differentiation via negative regulation between integrin α6β4 and the FAK‐PI3K signaling pathway.[47] Subsequently, this effect drives the elongation of ORS and failure to form the bulge, a quiescent niche essential for cyclical bouts of hair growth. The gene discussed is SCD; the disease is Huntington disease.