Although nonsense and missense PDE11A variants were found in 20% of patients with acromegaly, there was no significant difference in variant frequency compared with controls, suggesting that these variants are unlikely to contribute to the pathogenesis of GH-secreting adenomas since the conservation of the wild-type allele of PDE11A remains in the majority of tumor samples and no significant clinical phenotype could be observed in patients with variant PDE11A (13)