Mechanistically, 182 directly bound to STAT3 with high affinity by forming hydrophobic bonds at GLN247 and GLN326 residues, as well as hydrogen bonds at ARG325 and THR346 residues, interacted with STAT3 physically, and functionally inhibited the transcription activity of STAT3, thereby regulating atherosclerosis. The gene discussed is STAT3; the disease is atherosclerosis.