When oxidative stress or serum starvation occurs, cytoplasmic FOXO1 is acetylated at K262, K265, and K274 via SIRT2 dissociation, facilitating the interaction between cytosolic FOXO1 and ATG7 and the autophagic process, leading to tumor suppression in an autophagy-dependent manner.15,120 In response to Angiotensin II stimuli, HDAC4 expression is upregulated in vascular endothelial cells, which consequently deacetylates FOXO3a to transcriptionally activate autophagy, and therefore leads to vascular inflammation.121. Here, FOXO1 is linked to neoplasm.