Based on preclinical evidence that lithium activates AKT15 and inhibits GSK3β and PKCε8, we hypothesized that: (1) BD status and symptom severity at baseline would be directly associated with baseline mRNA levels of GSK3β and PKCε, but inversely related to baseline mRNA levels of AKT1; (2) lithium treatment would result in downregulation of mRNA levels of GSK3β and PKCε, and upregulation of mRNA levels of AKT1; and (3) lithium-associated transcriptional changes of these genes would be significantly associated with reduction in symptoms. Here, AKT1 is linked to Behcet disease.