phenotypes (Oberlin et al. 2011) and electrophysiological measures in the DS between replicates two and three are quite similar (Fritz et al. 2019), it remains possible that different replicates may not contain identical gene-sets which may limit the generalizability of our current findings. Lastly, the present study does not specifically probe how changes in the expression of these genes and phosphorylation patterns of peptides directly produces changes in neuronal function nor the maladaptive AUD-related behavior associated with HAP mice. Further studies are necessary to examine the hypotheses and speculations proposed herein. Nevertheless, this integrated mutli-omic analysis yielded bountiful intriguing differences between the HAP and LAP lines in the DS, and we encourage readers to carefully examine our full datasets for questions that may be of interest to them. These complementary and integrative -omics analyses may be a valuable resource that can inform future studies of basal gene and protein expression and phosphopeptide patterns in animal models of AUD.
