Interestingly, Dlk1 was re‐expressed in an autochthonous mouse model of ACC, in which concomitant inactivation of Trp53 and activation of Ctnnb1, driven by the aldosterone synthase promoter (BPCre) [8], leads to ACC formation with high penetrance. This evidence concerns the gene CTNNB1 and adrenal cortex carcinoma.