Autophagy inhibition is observed after AZT treatment and prevented myofibroblast differentiation through pro-fibrotic NOX4 suppression [12], however healthy fibroblasts have not been compared to IPF fibroblasts so far and the entire mechanism of anti-fibrotic effects of AZT is not fully understood. The gene discussed is NOX4; the disease is idiopathic pulmonary fibrosis.