Unlike previous studies in pancreatic cancer where ATP6AP1 depletion attenuated IL-1β secretion [25], our findings reveal a paradoxical outcome in HCC: chronic ATP6AP1 overexpression amplifies NLRP3 inflammasome activity, yet simultaneously fosters an immunosuppressive TME.This dichotomy mirrors the “double-edged sword” nature of pyroptosis, where transient inflammation may activate antitumor immunity, while sustained activation promotes exhaustion of cytotoxic T cells and M2 macrophage polarization [26–30]. Here, ATP6AP1 is linked to pancreatic neoplasm.