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Though it has been argued that courts should admit biogenetic evidence on psychopathy, no research to date has evaluated whether individuals with clinical psychopathy have consistent genetic correlates. The current study: 1) systematically reviewed all quantitative and molecular genetic studies of PCL-R psychopathy, and 2) assessed the quality and reproducibility of findings. Using PRISMA guidelines, we reviewed 1 heritability and 15 molecular genetic studies of PCL-R psychopathy. Sample characteristics, research design, and the main findings of each study were qualitatively synthesized according to candidate neurotransmitter systems. We also assessed broad metrics of study quality such as sample generalizability, accounting for environmental or clinical variability in analyses, and replication of effects. Heritability estimates for the facets of clinical psychopathy were low. Molecular genetic findings were inconsistent and mostly unreplicated. Further, replicated findings were contradictory; elevated dopamine metabolite levels observed in independent samples was qualified by a lack of association between a candidate dopamine polymorphism and PCL-R scores. Inconsistent findings may be related to issues with study quality. Though most studies had clear hypotheses and generalizable samples, few accounted for clinical complexity of those samples, environmental factors, or gene-environment interplay. The current review suggests that the genetic bases of PCL-R psychopathy are not robust enough for forensic application. Genetic findings in people with antisocial characteristics (violence, addiction, CU traits) may not generalize to those with PCL-R psychopathy. Though genetic bases for psychopathy are widely accepted, we found very little evidence for consistent genetic correlates when we systematically reviewed studies of legally relevant PCL-R psychopathy. [ABSTRACT FROM AUTHOR]