Treatment of lung cancer cells with CVB-D can significantly suppress the expression of p65, a transcriptional suppressor of BNIP3, and the downregulation of p65 can significantly relieve its inhibition on BNIP3 transcription upon CVB-D treatment and can cause enhanced expression of BNIP3, thus enhancing its interaction with LC3 and mediating mitophagy activation. This evidence concerns the gene BNIP3 and lung carcinoma.