Some limitations are noteworthy. Our African ancestry sample was under-powered; more data are needed, particularly in light of potential disparities that result from a majority of genetic studies focusing on European-ancestry populations.63, 64 We had little or no information regarding comorbid psychiatric disorders for the majority of PGC samples; however, we did conditional analyses to account for these and it made little difference. Information regarding lifetime cannabis exposure and the potency of cannabis used was scarce. Our estimates of genome-wide SNP-h2 were far lower than the h2 estimated from twin and family studies (0·07–0·12 vs 0·5–0·7). This discrepancy between pedigree-estimated heritability and SNP-heritability is common across essentially all substance use disorders, and might be due to low power, some heritability residing in variants too rare to be included in our GWAS, and insufficient coverage of optimal common-variant genomic coverage in available microarray data even after imputation. An additional limitation is that we did not do formal Mendelian randomisation65 analysis. To do this analysis, we would have needed to remove sample overlap between our cannabis use disorder GWAS and the other
