In breast cancer, Prx I suppressed ROS-induced AKT phosphorylation to inhibit cell proliferation [37]; In lung cancer, Prx I suppressed the ROS-induced ERK/cyclin D1 pathway to inhibit tumor growth [11]; In pancreatic cancer, Prx I modulated P38 activation to promote cancer-cell invasion [38]; In liver cancer, Prx I is an immediate and sensitive marker of oxidative stress. This evidence concerns the gene CCND1 and lung cancer.