Thus, SOX2 appears to be a tumor suppressor in this model.194 In ESCC model, Krt-5-driven transgenic SOX2 expression in basal progenitor cells triggers hyperplasia in esophagus and squamous cell carcinomas in the forestomach, particularly when cooperated with inflammation-mediated Stat3 activation in the latter case.195 In a genetically engineered mouse model of osteosarcoma, induced by dual deletion of RB and p53 in the mouse osteoblast lineage, SOX2 deletion dramatically delays and reduces the tumor formation, along with an extended lifespan. This evidence concerns the gene TP53 and neoplasm.