AKT1 and Hyperkeratosis: Additional lines of evidence include data from animal models, such as mice bearing a keratinocyte-specific PTEN null mutation which are characterized by epidermal hyperplasia and hyperkeratosis [23], mice with ablation of two of the three Akt isoforms, Akt1 and Akt2, which lack the stratum corneum and die neonatally, possibly because of defects in the skin barrier [24] and mice carrying an epidermis-specific deletion of mTOR which die shortly after birth due to impaired early epidermal differentiation and lack of a protective barrier development [25].