Moreover, we reported that Sirt5-mediated autophagic flux activation by desuccinylating OPTN K108su, which echoed past reports that Sirt5-induced deacetylation of lactate dehydrogenase B (LDHB) at the K329 site triggered hyperactivation of autophagy and colorectal cancer cell growth [41] and that Sirt5 could promote autophagic flux by affecting both the early and late stages of the autophagy process in osteosarcoma cells exposed to DNA damage [42]. Here, OPTN is linked to osteosarcoma.