In another study, immunohistochemistry and DNA sequencing were performed in PPNAD tissue (five with micronodules, three ACAs and one ACC the developed within an ACA) from nine patients (eight of them harbored PRKAR1A defects); accumulation of β-catenin was found in all PPNAD tissues while activating somatic CTNNB1 variants were found in two of the five macronodules but were absent from the micronodules and the contralateral adrenal gland [46]. The gene discussed is CTNNB1; the disease is primary pigmented nodular adrenocortical disease.