In a mouse model of cSCC, where activation of oncogenic KrasG12D in combination with Tp53 deletion in the hair follicle lineage (using Lgr5-CreER/KrasG12D/Tp53KO mice) results in a wide spectrum of cSCC ranging from well-differentiated cSCCs to tumours resembling spSCC, YAP/TAZ were demonstrated to be essential for tumour initiation [139]. This evidence concerns the gene WWTR1 and neoplasm.