Autophagy, which is essential for homeostasis, can not only inhibit senescence, but can also promote SASP synthesis and induce senescence.41 Autophagy mediated by p38α promoted senescence in cancer cells, which confirmed that LC3II, an autophagy marker, was upregulated in senescent cells.42 We confirmed that LC3II levels were increased during senescence and decreased after treatment with GLS1 inhibitors and GLS1 knockdown in WJ-MSCs. The gene discussed is GLS; the disease is cancer.