Genetic mutations predominantly present in each primary adrenal hyperfunction, such as ARMC5 (hypercortisolism), CACNA1D (aldosteronism), and AIP (hyperandrogenism), disrupt key molecular pathways, including the cAMP/PKA/CREB signaling pathway and Wnt/β-catenin signaling, leading to uncontrolled hormone synthesis and tumorigenesis. Here, CREB1 is linked to adrenal gland hyperfunction.