of heroin abusers (52); and NEAT2, MIAT, MEG3 and EMX2OS were elevated in the NAc of cocaine abusers (52); smokers had dramatically elevated H19 expression in airway epithelium (53); demethylation of H19 was correlated to chronic alcohol use in males (54); and many LncRNAs played roles in cocaine-induced neural plasticity in NAc and risk for cocaine dependence (48). Therefore, we also explored the LncRNAs proximate to the risk genes in this study. Interestingly, a large antisense-overlapping LncRNA (>200k nt) covers ADHs 5, 4, 6 and 1A. Fourteen SNPs located within this LncRNA were associated with alcohol dependence. Such an LncRNA frequently uses diverse transcriptional and post-transcriptional gene regulatory mechanisms to carry out a wide variety of biological roles (47). It usually has a tendency to undergo fewer splicing events and typically shows lower abundance than sense mRNA transcripts (55). Additionally, a second smaller sense LincRNA (1,055 nt) is located between ADH4 and ADH6. Such an LincRNA usually collaborates with chromatin modifying proteins (PRC2, CoREST and SCMX) to regulate expression of proximate genes (56). Accordingly, we can postulate that these LncRNAs within ADH cluster might regulate the expression of the ADH genes and might be functional components of the pathways through
