Given the lack of T cells in nude mice, the GSDMC-increased sensitivity of tumor cells to PARPi in vitro may be offset by HMGB1-fueled tumor cell proliferation in nude mice, while in immunocompetent BALB/c mice, HMGB1-enhanced cytotoxicity of T cells may overcome the tumor proliferation-promoting effect of HMGB1, suggesting the dominant role of T cell–mediated antitumor immunity in response to PARPi treatment in normal immunocompetent mice. The gene discussed is HMGB1; the disease is neoplasm.