1999 Nature America Inc.• http://genetics. nature. com correspondence nature genetics• volume 23• november 1999 269 and Scd2, a functional SCD and its pseudogene exist in humans11. We are unaware of a direct parallel between the ab mutation and a human disorder, but the small sebaceous glands and the associated scarring alopecia of mutant mice are reminiscent of some of the clinical scarring alopecias12. We conclude that abJ and ab2J mice lack Scd1 expression because of their genomic deletions in Scd1; hence they can serve as models for Scd1 deficiency. Specific expression of Scd1 in wild-type sebaceous glands and the cutaneous pathology seen in the mutant mouse demonstrate the importance of Scd product (monounsaturated fatty acids) to normal sebaceous gland function in relation to hair. Although the exact mechanism is unclear at present, fatty acids are known mediators of signal transduction13, 14 and have been implicated in acne15. As these mice also suffer from corneal opacities and hypoplastic meibomian glands, the importance of Scd1 to normal ocular barrier function is also worth noting.