Intriguingly, in Krt15-CrePR; LSL-KrasG12D; Ptenwt/flox; LSL-tdTomato mice, tumor growth significantly increased in the context of Pten loss of function; however, the incidence of oncogenic Ras/Pten-mediated foregut tumor formation was consistently higher from Krt15+ basal progenitors resident to the region adjacent to the SCJ, consistent with the p53 loss model (Fig. 3c–e, Supplementary Fig. 3). Here, KRT15 is linked to neoplasm.