The choline transporter CTL1 is highly expressed in macrophage-like and fibroblast-like synoviocytes in the synovia and cartilage of patients with RA, and deficient choline uptake through CTL1 in macrophages reduces IL-1β production via attenuation of mitochondrial ATP synthesis, which drives activation of AMPK-mediated mitophagy and termination of NLRP3 inflammasome activation [75, 76]. The gene discussed is NLRP3; the disease is rheumatoid arthritis.