Sorry for the double reply, but I just read the sources cited in your quote. The content of the studies differs significantly from the Wikipedia author's descriptions.

The first study, which "failed to find any large or statistically significant effects of the MAOA gene on aggression", actually did find one statistically significant link between male MAOA gene expression and violence [0]:

>For studies with categorical outcomes (Supplementary Figure 1), the following associations were found: (1) COMT-Val158Met was significantly associated with violence (P=0.02) as a categorical outcome; (2) when examining violence as a categorical outcome only, there was an association for MAOA promoter 30 bpVNTR in males with a history of violence (P=0.023)

The second study isn't cited correctly. The results are taken from another study cited in the one listed [1]. The results of that study are intriguing, as they do fail to find a link between MAOA and violence in a GWAS of 4816 individuals. However, their data on subjects' violent behavior comes entirely from self-reported questionnaires.

This study also lumps the 3-repeat MAOA allele in with the 2-repeat allele variant. This is a common confounding factor in studies on violence and MAOA [2]. MAOA-3R is far more common in the populations of all racial/ancestral groups compared to the 2-repeat allele, and its measured effect on aggressive behavior is much smaller. Defining L-MAOA, or the low-activity MAOA gene as both MAOA-3R and MAOA-2R dilutes the value of any study on the 2-repeat allele, which is the specific allele I brought up in my first comment.

The third study, which "failed to find any evidence in a large GWAS", found highly significant effects in their candidate study while the GWAS was hampered by a lack of data [3]:

>Therefore, it is plausible that while research of the genetic background of criminal or violent behavior is hampered by many confounding factors, focusing on extreme phenotypes might yield more robust results. This was demonstrated in our analysis on the association between rs11649622 and MAOA genotypes vs the number of committed violent crimes, showing clear dose–response effects. However, collecting data from extreme phenotypes is difficult. For this reason, our number of study subjects was relatively small, which resulted in a rather low statistical power in the GWAS.

>Concerning statistical significance, the P-value of 2.9 × 10−5 for the low-activity MAOA variant can be considered as extremely significant, as the Bonferroni-corrected level of significance in the candidate gene study was 0.025.

>The results indicate both low monoamine metabolism and neuronal membrane dysfunction as plausible factors in the etiology of extreme criminal violent behavior, and a conservative estimate implies that 5–10% of all severe violent crime in Finland is attributable to specific MAOA and CDH13 genotypes.

The last study, which "failed to reveal robust evidence of MAOA in aggression", actually ranked MAOA first as a risk factor for aggressive behavior [4]:

>Also, individual genes were ranked based on their cumulative weights to quantify their importance as risk factors for aggressive behavior, which resulted in 40 top-ranked and highly interconnected genes.

>Supplementary Table 4 lists all the 1767 genes from the eight aggression gene sets (adult and children GWAS, transcriptomics in four rodent models, KO mice and OMIM) and ranks them based on their number of occurrences and weighted ranks for aggression (only human orthologs were included from the rodent genes). MAOA was ranked highest with both methods.

Ultimately, I'm inclined to believe those meta-analyses which do find an effect on MAOA-2R and agression because the mechanism of action of this gene is not entirely a mystery. Low-repeat versions of the MAOA allele result in less MAOA in the brain. We know what severe MAOA deficiency looks like; it's called Brunner syndrome [5]. Symptoms include violence, agression, and impulsive behavior. I think it's reasonable to hypothesize a continuum of increased aggression between normal MAOA levels and the extreme lows of Brunner syndrome.

[0] https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC3965568/

[1] https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC5048197/

[2] https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC4369574/

[3] https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC4776744/

[4] https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC6274606/

[5] https://en.wikipedia.org/wiki/Brunner_syndrome