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Mitochondrial membrane potential decreases after damage, making PTEN-induced Kinase1 (PINK1) accumulate and phosphorylate ubiquitin at Ser 65 in the outer mitochondrial membrane, which then recruits and binds Parkin proteins, thereby activating E3 ligase, resulting in more ubiquitination of outer mitochondrial membrane proteins, further driving the binding of ligands such as the autophagy adaptor protein Sequestosome 1 (PSQSTM1/P62), and finally making the autophagosome fuse with the damaged mitochondria to complete the mitochondrial autophagy process ( Studies have shown that mitophagy can lead to cisplatin resistance during tumor chemotherapy, thereby reducing antineoplastic efficacy

However, the results from several studies attempting to establish a relationship between the GSTM1 null genotype and the risk of incidence of lung cancer in various ethnic populations have been conflicting [9] which could suggest that the GSTM1 null variant has only a marginal impact on the genetic susceptibility to tobacco-related cancers [10]