CYP11B2 and hyperaldosteronism: By utilizing in situ hybridization method, Shigematsu et al. (49) reported the presence of APCC-like subcapsular micronodules, showing intense transcript expression for HSD3B2, CYP11B1, and CYP11B2, but not CYP17A1, implying that the nodules have the steroidogenic enzymatic property needed to synthesize aldosterone and thus might be responsible for hyperaldosteronism.