Although both the protist T. muris and the helminth N. brasiliensis have been shown to produce succinate (Nadjsombati et al., 2018), Sucnr1-deficient mice were incapable of clearing the protist infection, but were able to expel N. brasiliensis worms even in the absence of Sucnr1 (Lei et al., 2018; Nadjsombati et al., 2018), suggesting redundancy and involvement of additional receptors. The gene discussed is SUCNR1; the disease is infection.