In agreement, genetic deletion or pharmacological inhibition of ATX significantly attenuated modeled arthritis [10], bleomycin-induced lung fibrosis [11], hepatic fibrosis/hepatocellular carcinoma [12], obesity-induced hepatic steatosis [21] and resistance to chemo- or radiotherapy [22] in different experimental animal models, thus establishing ATX as a possible therapeutic target in chronic inflammatory diseases. The gene discussed is ENPP2; the disease is fatty liver disease.