Furthermore, LaCl3 inhibited the exaggerated LPS-induced TNF-α synthesis observed in monocytes and neutrophils of human CGD patients and it also increased the survival rates of APO-treated mice submitted to CLP, providing clear evidence for the in vivo efficacy of targeting the Nox2/TRX-1/NF-κB pathway. The gene discussed is NFKB1; the disease is chronic granulomatous disease.