Interestingly, lysosomal disrupting reagents such as bafilomycin A1 (Baf A1), an inhibitor of vacuolar-type H+-ATPase that prevents the re-acidification of acidic organelles, or glycyl-phenylalanine-2-naphthylamide (GPN), a reagent that osmotically ruptures lysosomes, also inhibited NK cells from inducing ADPR production in response to tumor PME stimulation (Fig. 4c). The gene discussed is ATP6V1A; the disease is neoplasm.