Recent studies have demonstrated that inhibition, silencing, or KO of several mitochondrial components, including POLRMT, ADCK2, TNF receptor-associated protein 1 (TRAP1) and YME1L, led to mitochondrial dysfunction, resulting in reduced energy production, increased ROS production, oxidative injury, and apoptosis in NSCLC cells [24–27]. This evidence concerns the gene TRAP1 and non-small cell lung carcinoma.