Although obsessive-compulsive disorder (OCD) is highly heritable and genetically correlated with numerous psychiatric and behavioural traits, it remains unclear whether these associations persist after accounting for shared genetic variance. This study applied genomic network analysis and statistical attenuation testing to compare marginal and conditional genetic correlations between OCD and eight comorbid traits: anxiety disorders, anorexia nervosa, Tourette syndrome, attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), posttraumatic stress disorder (PTSD), major depression, and neuroticism. This genomic network was then integrated at the SNP and gene level to identify unique and pleiotropic genetic effects. All traits showed statistically significant bivariate genetic correlations with OCD, with the strongest correlation being with anxiety disorders. PTSD and major depression were excluded due to multicollinearity with anxiety disorders. Of the remaining traits, only anxiety disorders, anorexia nervosa, and Tourette syndrome exhibited statistically significant conditional genetic correlations with OCD once shared variance was accounted for. In contrast, ADHD and neuroticism were indirectly linked to OCD through anxiety disorders in the sparse genomic network. Despite showing no evidence of attenuation, ASD’s conditional genetic correlation with OCD was not significant, likely reflecting limited power in the ASD GWAS. At the SNP and gene levels, few unique associations reached significance: only anorexia nervosa and ADHD displayed significant unique SNPS, and no unique genes emerged for OCD or anxiety disorders. Collectively, these findings indicate pervasive pleiotropy across psychiatric disorders, particularly between OCD and anxiety disorders. This research highlights the importance of transdiagnostic approaches to psychiatry rather than frameworks focusing on disorder-specific risk. Ongoing analyses are currently being conducted using transcriptome-wide association studies to clarify the brain tissues and neural circuitry involved in the shared and unique genetic liability discovered in this research.