Although phase III clinical trials did not demonstrate any improvement in the prognosis of NSCLC patients treated with DMXAA in combination with standard chemotherapy [60], researchers have revealed that the expression levels of TNF-α, IFN-β, and STING were significantly up-regulated in EML4-ALK NSCLC tumors after DMXAA treatment, which resulted in the inhibition of tumor growth and the induction of strong anti-tumor immunity in EML4-ALK NSCLC mouse models [61]. The gene discussed is ALK; the disease is neoplasm.