A very recent study identified a role for CR3 in activation of the microglial NADPH oxidase (Nox2) and subsequent neurodegeneration in a toxin-induced PD model; CR3 knockout mice were protected from dopaminergic neuron loss and motor dysfunction, suggesting that complement opsonization and CR3 engagement contribute to the disease process (69). The gene discussed is CRIPTO3; the disease is Parkinson disease.