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). This evidence concerns the gene SENP1 and neoplasm.