In cancer cells persistently expressing NLRP11, KAT7 tends to translocate from the nucleus to the cytoplasm and is recruited to bind with vimentin by NLRP11, resulting in vimentin acetylation at K104 and inhibition of ubiquitin‐independent proteasomal degradation, thereby contributing to the malignant phenotype related to epithelial–mesenchymal transition in LUAD cells. Here, VIM is linked to cancer.