Deregulation of the regulatory mechanisms that operate in healthy skin to control YAP/TAZ leads to their hyperactivation in skin cancers: Conditional knockout of αE-catenin in the HF bulge (using GFAP-Cre mice) was found to cause development of early onset keratoacanthomas displaying increased nuclear abundance of YAP [101], and there is significant correlation between low αE-catenin abundance and nuclear YAP localisation in human keratoacanthomas and cSCC [99,101]. This evidence concerns the gene GFAP and keratoacanthoma.