Since alcohol‐exposed neuron cultures exhibited an increase in KCNJ6 expression, artificially increasing KCNJ6 expression permits investigation of regulated cellular mechanisms. Differences in KCNJ6/GIRK2 expression alone are predicted to be sufficient to alter the effects of alcohol on neuronal function, including spiking activity and associated energy utilization. For this approach, using an isogenic cell line strategy where variable genetic backgrounds are retained provides a complementary means of inquiry to SNP‐specific findings. Current efforts in COGA aim to capitalize on lentiviral expression and CRISPRa technology to dissect KCNJ6 influence on neuronal function, independently of the myriad factors involved in AUD.
