For the associations reported in the second stage of this work, key shortcomings include a relatively small sample size, reliance on estimates of the prevalence of depression rather than direct epidemiological research, the possibility that other confounding factors may have been overlooked in the analysis, the limitations of inferring causation from population-level associations [173], and our lack of knowledge regarding the functional consequences of the MLN polymorphism being analyzed, particularly in terms of gut–brain axis functioning. The gene discussed is MLN; the disease is depressive disorder.