Individual SNPs on chromosome 8 are eQTLs for CHRNA2 and EPHX2, extending previous work by Demontis and colleagues3 in iPSYCH, with replication in the deCODE data. Note that iPSYCH and deCODE are the main contributors to this finding in the meta-analysis (piPSYCH=5·73 × 10−8, pdeCODE=0·0003, pPGC=0·06; appendix p 23). A large GWAS of schizophrenia54 has also implicated this variant (p=3·68 × 10−6), but conditioning for top schizophrenia loci did not modify the association with cannabis use disorder (p=4·33 × 10−8; appendix p 18). Given the role of CHRNA2 variants in tobacco smoking,36 it is plausible that the findings for cannabis use disorder and schizophrenia are partially driven by the high rates of tobacco use in those populations.55 However, conditioning cannabis use disorder on the GWAS of cigarettes per day increased the significance of the lead variant rs4732724 (p=4·16 × 10−9; appendix p 18), although a different SNP was identified as the lead SNP (rs11783093). When rs11783093 was conditioned for the GWAS of smoking initiation, the signal was attenuated (p=1·55 × 10−6; appendix p 18). These findings suggest that the chromosome
