Autophagy-deficient cells are impaired in DNA repair by the error-free process of homologous recombination. Cells lacking autophagy machinery largely depend on the non-homologous end joining, the error-prone repair process of DNA double-strand breaks. Sustained reliance on non-homologous end joining results in loss of genetic integrity.50 Interestingly, Gene Set Enrichment Analysis analysis indicate that high expression miR-20a is associated with reduction in the levels of proteins involved in DNA repair pathways (data not shown). Thus, we propose that in cancers with higher miR-20a, there is parallel inactivation of autophagy and impairment of DNA repair; this may impair the ability of the cells to adapt to environmental stress, which may subsequently enable gene amplification, mutation and accumulation of DNA damage, thereby promoting genomic instability and cancer progression. Future work should address these questions.