Because a basal mitochondrial function is required for cancer cell survival and tumor growth (e.g., generating chemical building blocks for biosynthesis) [4, 5], upregulation of PGC1α-mediated mitochondrial biogenesis may play a critical role in meeting such a requirement, particularly in the case of augmented mitochondrial turnover (mitophagy) induced by Drp1. Here, DNM1L is linked to neoplasm.