Similarly, patient-derived ESCC tissues with a high abundance of Fn had higher CYP1A1 protein levels than those with low Fn. In addition, inhibition of CYP1A1 either genetically using the shRNA lentivirus vector or pharmacologically using CH223191 abolished the effects of Fn on cell proliferation and colony formation in vitro and tumor growth in vivo [71]. The gene discussed is CYP1A1; the disease is esophageal squamous cell carcinoma.