A recent study reported that MAOA is subject to X-inactivation using a measure of allelic expression imbalance in human brain tissue concluded that there was no evidence for skewing in normal individuals (Pinsonneault et al. 2006). Furthermore, a recent study of functional response of MAOA genotype for amygdala and cingulate volume demonstrated the functioning of heterozygous females to be in between that of the homozygotes (Meyer-Lindenberg et al. 2006). Therefore, in the presence of inconsistency on whether MAOA is subject to X-inactivation, the inclusion of the additive effects of MAOA genotype on risk to CD is appropriate and consistent with the majority of findings reported in recent molecular and neuroscience literature.
