The integration of kinase (PKA, CDK5, GSK3) and small G-protein (IQGAP1) signalling pathways through CaMKK2, all of which have demonstrated links with human bipolar disorder, points to the possibility that bipolar disorder is a signalopathy that stems from defects in this signal transduction network, and potentially explains the clinical heterogeneity and polygenic nature of the condition. This evidence concerns the gene CAMKK2 and bipolar disorder.