ASAH2 and neoplasm: Su et al. reported that the excessive upregulation of β5-integrin in solid tumors could activate Src-STAT3 signaling to promote N-acylsphingosine amidohydrolase 2 (ASAH2) activity, which would reduce the cellular abundance of its metabolite ceramide and sequentially alleviate ROS stress in tumor cells through regulating mitochondrial metabolism, thus protecting tumor cells from treatment-induced pyroptosis by blocking the NLRP3-caspase 1 axis.