These models include adenosquamous carcinomas driven by combined loss of Pten and Smad4 [23], mucinous adenocarcinomas resulting from overexpression of Kras on a Nkx2.1 haploinsufficient background [24] and SCC following loss of the key tumor suppressors Lkb1 and Pten [25]. This evidence concerns the gene PTEN and neoplasm.