Possible explanations could be that: (1) through the hypoxia-induced factor-1α (HIF-1α) signaling pathway, SENP1 could promote the proliferation of NSCLC cancer cells, resulting in larger tumor size; (2) SENP1 could regulate matrix metalloproteinase-9 (MMP-9) to promote NSCLC cancer metastasis; meanwhile, SENP1 might enhance NSCLC cell invasive ability via modulating epithelial–mesenchymal transition marked genes, which contributed to the occurrence of lymph node metastasis (22, 24). The gene discussed is SENP1; the disease is non-small cell lung carcinoma.