[10] The epigenetic modification of MAOA gene expression through methylation likely plays an important role in women.

[14] Monoamine oxidase A catalyzes O2-dependent oxidation of primary arylalkyl amines, most importantly neurotransmitters such as dopamine and serotonin.

The products are the corresponding aldehyde, hydrogen peroxide, and ammonia: This reaction is believed to occur in three steps, using FAD as an electron-transferring cofactor.

[15][16] Compared to MAO-B, MAO-A has a higher specificity for serotonin and norepinephrine, while the two enzymes have similar affinity for dopamine and tyramine.

"[21] MAO-A levels in the brain as measured using positron emission tomography are elevated by an average of 34% in patients with major depressive disorder.

[26] Other studies failed to find a significant relationship between high-activity variants of the MAOA gene and major depressive disorder.

[27][28] In patients with major depressive disorder, those with MAOA G/T polymorphisms (rs6323) coding for the highest-activity form of the enzyme have a significantly lower magnitude of placebo response than those with other genotypes.

[29] In humans, an association between the 2R allele of the VNTR region of the gene and an increase in the likelihood of committing serious crime or violence has been found.

The VNTR 2R allele of MAOA has been found to be a risk factor for violent delinquency, when present in association with stresses, i.e. family issues, low popularity or failing school.

[36] High testosterone, maternal tobacco smoking during pregnancy, poor material living standards, dropping out of school, and low IQ predicted violent behavior are associated with men with the low-activity alleles.

[37][38] According to a large meta-analysis in 2014, the 3R allele had a small, nonsignificant effect on aggression and antisocial behavior, in the absence of other interaction factors.

[40] A study of Finnish prisoners revealed that a MAOA-L (low-activity) genotype, which contributes to low dopamine turnover rate, was associated with extremely violent behavior.

[44] This lack of replication is predicted from the known issues of candidate gene research, which can produce many substantial false positives.

[55] Judges in Germany are more likely to sentence offenders to involuntary psychiatric hospitalization on hearing an accused's MAOA-L genotype.

[64] There is research in both humans and mice to support that a nonsense point mutation in the eighth exon of the MAOA gene is responsible for impulsive aggressiveness due to a complete MAO-A deficiency.