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). This evidence concerns the gene PDE11A and neoplasm.