For example, SEMA3B was elevated in methotrexate‐induced cell senescence models.29 In lung cancer, wild‐type SEMA3B inhibited tumor growth by promoting apoptosis.30 The researchers also found that SEMA3B promoted apoptosis in breast cancer cells.31 Therefore, we considered that the regulation of EFEMP1 on HCC cells may be through SEMA3B based on the previous experiments. This evidence concerns the gene SEMA3B and lung carcinoma.