For instance, the adrenocortical tissue-specific expression of a gain-of-function β-catenin variant in combination with Trp53 (the murine homologue of TP53) deletion resulted in the development of metastatic and hormonally active adrenocortical carcinoma, which shares similar gene expression profiles with primary human adrenocortical carcinoma [151]. This evidence concerns the gene TP53 and adrenal cortex carcinoma.