For further analysis, we selected ATP6V0C, which encodes a critical component of an ATP-driven proton pump V-ATPase and regulates functional autolysosome formation and the acidic tumor microenvironment.27,40 Genetic depletion of ATP6V0C disrupted lysosomal acidity and blocked autophagic flux, thereby generating non-functional autolysosomes.41 V-ATPase is upregulated in hepatocellular carcinoma42 and knockdown of ATP6L blocked the metastasis of hepatocellular carcinoma in a xenograft model.43 This evidence concerns the gene ATP8A2 and neoplasm.