Chandimali et al. [90] further show that Prx2 knockdown in gefitinib-resistant NSCLC CSCs raises ROS and apoptosis, and suppresses sphere formation, migration, invasion and angiogenic signaling; miR-122–mediated PRX2 silencing similarly elevates ROS/apoptosis but more strongly shuts down Wnt, Hedgehog and Notch pathways, thereby abolishing CSC traits and tumor growth. The gene discussed is PRDX2; the disease is neoplasm.