There are two possible explanations for this: first in the in vitro studies, we did not observe complete menin loss as is seen in the Men1+/− mouse tumours, and therefore the residual menin expression may be attenuating the phenotype or second the menin-null tumours may accumulate additional mutations that can further alter miRNA expression, potentially by modifying the allelic imbalance of miR-15a-miR-16-1 expression, as reported in CLL (Veronese et al. 2015). The gene discussed is MEN1; the disease is neoplasm.