The mechanistic integration of the findings regarding the renal protection (i.e., GSK-3beta, WNT/beta-catenin, cyclic AMP), the polydipsia (i.e., cyclic AMP, GSK-3beta), coat color considerations (i.e., melanocortin/leptin pathway), obesity (i.e., leptin/melanocortin pathway), sex differences in lithium action (i.e., sex hormones and puberty-related events, GSK-3beta, leptin, and the immune dysfunction (i.e., leptin/melanocortin pathway, GSK-3beta, WNT/beta-catenin) attributes provide an attractive constellation of potential biomolecular mechanisms for assessing lithium actions in one model. The gene discussed is CTNNB1; the disease is obesity due to melanocortin 4 receptor deficiency.