Recent studies indicate that certain cells express gasdermin E (GSDME, also called deafness autosomal dominant 5), which is specifically cleaved by activated caspase-3, and that the resulting N terminal of GSDME (Gsdme-N) then forms pores in the cell membrane and switches apoptosis to pyroptosis in response to caspase-3 triggers, such as chemotherapeutic drugs, tumor necrosis factor and viral infection [22,23]. This evidence concerns the gene CASP3 and autosomal dominant nonsyndromic hearing loss.