To examine the functional impact of autophagy triggered in response to HNK, we blocked autophagy in HNK-treated breast cancer cells by inhibiting autophagosome formation using 3-methyladenine (3MA), a phosphatidylinositol 3-kinase (PtdIns3K/Vps34) inhibitor30, or impeding autophagosome-lysosome fusion using Baf, a specific vacuolar type H+-ATPase inhibitor31 or increasing lysosomal pH using chloroquine, a weak base. The gene discussed is ATP6V1A; the disease is breast cancer.