out of many does not account for the influence of other genes that affect alcohol sensitivity and consumption, or possible bias due to genome wide polygenic effects. For example, genetic polymorphisms of GABAA -α2 receptors, and GABAA-α6 receptors, nicotinic acetylcholine receptors, serotonin receptors, and the serotonin transporter have been reported to affect alcohol response (for review see Uhart et al., 2013, Radel and Goldman, 2001, Ray et al., 2016). It is also important to consider that other OPRM1 and DAT1 gene variants may also contribute to individual differences in alcohol response, and that nonsystematic variations in genotype frequency, sampling techniques, and variation in LD structure with other risk loci across studies may be significant factors. Fifth, the laboratory cumulative alcohol dosing procedure also may affect subjective responses. The procedure used a standard volume drink containing Kool-Aid and grain alcohol, with each drink consumed within 10 minutes, and drinks administered at regular intervals over 2 hour period. While these procedures permit blinding of the placebo drink, controlled dosing and BAC achieved, drinks are less palatable than an individual’s preferred drink, and the timing of consumption may be slower or faster than it would be in the natural environment. Despite these caveats,
