In line with our results, Lei et al also revealed that knockdown of CDR1as could work as an oncogene in HCC via the suppression of HCC cell proliferation and invasion through targeting miR‐7.21 Bax/Bcl2 and cleaved‐Caspase‐3/Caspase‐3 are commonly used indicators of apoptosis.35 Interestingly, CDR1as up‐regulated the Caspase‐3 activity and apoptosis of cells, while overexpression of miR‐7a reversed CDR1as‐induced phenotypes, leading to decreased Caspase‐3 activity and apoptosis,36 which were consistent with our findings. The gene discussed is BCL2; the disease is hepatocellular carcinoma.