Alternatively, as studies aimed at understanding the molecular pathogenesis of bipolar disorder have not yet implicated CCN3 abnormalities, and as brain levels of CCN family proteins (and interactors) fluctuate considerably across mammalian pregnancy and the postpartum period [78], it is plausible that it is specific abnormalities in the expression/function of these proteins that confer PP risk. This evidence concerns the gene CCN3 and bipolar disorder.