In particular, Eprin-B1/EphB2 signaling promotes spine development by activating RAC1 through TIAM1, while NMDA-mediated calcium influx at glutamatergic synapses activates a CAMK2 (calcium/calmodulin-dependent protein kinase II)-TIAM1 complex that persistently activates RAC1, leading to LTP and spine enlargement [207,208]; interestingly, knock-in mice harboring a mutation that inhibits the formation of the CAMK2–TIAM1 complex showed reduced RAC1 activity and memory deficits [209]. The gene discussed is RAC1; the disease is memory.