Alk is regulated by the gene LIM-domain only (Lmo), which is implicated in sensitivity to the sedative effects of ethanol in flies (Lasek et al. 2011a). Based on the observation that Alk was down-regulated in Lmo mutants, Alk was examined to determine whether it also influenced the sedative effect of ethanol. Indeed, flies with mutant alleles of Alk show diminished behavioral sedation in response to ethanol (Lasek et al. 2011b). Next, this team investigated the mouse homolog of Alk, and observed correlations between gene expression and several ethanol-induced behaviors in a recombinant inbred panel of mice. To determine whether these correlations were causative, they generated an Alk knock out mouse, which showed diminished sensitivity to the sedative effects of ethanol in the loss of righting reflect task as well as higher voluntary ethanol drinking in the drinking-in-the-dark paradigm (Lasek et al. 2011b). Finally, the same authors studied several SNPs in the human ALK gene and showed a nominally significant association between these SNPs and altered physiological and subjective responses to ethanol in humans (Lasek et al. 2011b). Such responses have
