GSDMD and ductal breast carcinoma in situ: We found that disulfiram, a potent inhibitor of pyroptosis by blocking gasdermin D (GSDMD) pore formation [51], completely suppressed the death of DCIS-Snai1-ER EMT cells under glucose starvation, whereas ferrostatin (a ferroptosis inhibitor) and necrostatin (a necroptosis inhibitor) had a mild and no effect on cell viability, respectively (Figure 8A).