For instance, Gpr18 and RvD2 were shown to be upregulated in human coronary arteries in presence of atherosclerotic lesions; and the treatment of ApoE-deficient hyperlipidemic mice with the Gpr18 antagonist O-1918 was shown to reduce atherosclerosis (Bardin et al., 2022). The gene discussed is GPR18; the disease is atherosclerosis.