It was shown in a mouse model of SCC that the enhanced mTOR (a mammalian target of rapamycin) signaling obtained in keratinocytes by deletion of Pten (phosphatase and tensin homolog deleted on chromosome 10) strongly enhanced the level of Fgf10 protein, and Pten deletion-induced skin cancers were inhibited by epidermal Fgfr2 deletion [86]. Here, PTEN is linked to skin neoplasm.