There is emerging evidence that sub-optimal expression of GSDME, at least in some cancers, is due to hypermethylation of its promotor: Ibrahim et al. identified key sites of GSDME hypermethylation in colorectal cancer cells but not normal colorectal tissue (87), drawing fresh attention to an early study that showed demethylation by 5-aza-2’-deoxycytidine restored GSDME induction in a breast cancer cell line (88). Here, GSDME is linked to breast carcinoma.