Our study indicated that, on the one hand, CD44s were positively associated with caspase-1/IL1B pathway, and targeting CD44s promoted p62-mediated degradation of caspase-1 through activating AMPK/mTOR signaling and then decreased IL1B release in normoxia conditions, which contributed to the impairment of EMT phenotype and tumor proliferation. This evidence concerns the gene MTOR and neoplasm.