The recognition that β-catenin dysregulation is responsible for ACP have led to two conflicting mouse models for the formation of ACP – in mice an ACP-like tumor can develop from targeted CTNNB1 mutations in either pituitary oral ectoderm precursors in developing mice embryos or in pituitary stem cells in post-natal mice [46]. This evidence concerns the gene CTNNB1 and neoplasm.