AKT1 and schizophrenia: In recent work using a B lymphoblast cell model, we showed that B lymphoblasts express erbB2 and erbB3 receptors, and that NRG1α signals through these receptors via the PI3K/Akt and PLC pathways in order to promote chemotactic migration.[7] We also found that genetic variation both in NRG1 and COMT previously associated with schizophrenia predicted the migratory response of these cells to NRG1, suggesting a potential cellular mechanism for the genetic association to the disorder.