Mutations in Krt17 and Krt16 are associated with Palmoplantar Keratoderma (PPK) lesions (i.e. abnormal thickening of palm skins) in humans [50], and mice that lack the Krt16 gene develop spontaneous lesions resembling human PPK [51]. This evidence concerns the gene KRT17 and epidermolytic palmoplantar keratoderma, 1.