In a word, overexpression of GSDME could be automatically cleaved into N-GSDME in cytoplasm and bind to mitochondria to perforate it, contributing to mitochondrial damage decreasing its potential and the release of mtDNA from mPTP, which activated the cGAS-STING pathway to promote IFNβ expression level and enhance the number of CD8+T cells to secret more Il2, TNFα, GZMB, and PFN to cleave GSDME into N-GSDME in tumor cells causing pyroptosis, which led to the release of mIL1β and mIL18 in TME (Fig. 9). Here, CGAS is linked to neoplasm.