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. Here, CDK5 is linked to bipolar disorder.