Somatic mutations, including KCNJ5, ATP1A1, ATP2B3, CACNA1D, CACNA1H, CLCN2, and CTNNB1 have been discovered in more than 90% of APAs.125,126 The first 6 mutations trigger aldosterone secretion by activating the intracellular calcium signalling pathway, while CTNNB1 encodes β-catenin, a protein in the Wnt/β-catenin signalling pathway, involved in adrenal cortex maintenance, adrenal steroidogenesis, and adrenal tumourigenesis.7 The constitutive activation of β-catenin in mouse models caused ZG hyperplasia and hyperaldosteronism. This evidence concerns the gene CTNNB1 and hyperaldosteronism.