It has also been reported that reduced editing of COPA, an important paralog of COPB2, has been implicated in the pathogenesis of HCC, and editing of COPAWT may switch it from a tumor-promoting gene to a tumor suppressor by deactivating the PI3K/AKT/mTOR pathway through downregulation of caveolin-1 (CAV1) [20]. This evidence concerns the gene CAV1 and neoplasm.