Specifically: 1) Lithium has been shown to increase the expression of the anti-apoptotic gene BCL2 with reduction of the expression of the pro-apoptotic genes p53 and Bax (Chen et al., 1999) clearly indicating a role in influencing the molecular cascade regulating the programmed cell death. This evidence acquires particularly interest in light of recent findings on BCL2. Two recent studies (Machado-Vieira et al., 2011, Uemura et al., 2011) demonstrated that, in individuals with BD, BCL2 gene expression regulated by the single nucleotide polymorphism (SNP) rs956572 directly impacted intracellular Ca2+ homeostasis dysregulation, a molecular signalling pathway proved to play a significant role in the pathogenesis of BD. 2) Using a genome wide gene expression approach (GWGE) on multiple prostate human cancer cell lines that were incubated with lithium, Sun and coworkers 11 showed a marked downregulation of genes involved in DNA replication. In another study, Seelan et al. (2008), in the attempt of profiling the lithium-modulated gene expression in human neuronal cells with microarray, identified peroxiredoxin 2 (PRDX2), an antioxidant enzyme, as the most upregulated gene, and tribbles homolog 3 (TRB3), a pro apoptotic protein, as the most downregulated, further suggesting a role of these pathways in the mood stabilization process.