Three researchers demonstrated that the knockdown of Txnrd1 resulted in decreased Txnrd1 and oxidative stress in human CML cells [40]; the knockdown of Txnrd2 decreased Txnrd2, CAT, SOD, and GPx, as well as caused oxidative stress in NSCLC cells [41]; the knockout of Txnrd3 aggravated nickel-induced cardiac oxidative stress in mice [42]. The gene discussed is SOD1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.