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Reported triggers of eryptosis include osmotic shock, oxidative stress, energy depletion, ceramide, prostaglandin E<jats:sub>2<\/jats:sub>, platelet activating factor, hemolysin, listeriolysin, paclitaxel, chlorpromazine, cyclosporine, methylglyoxal, amyloid peptides, anandamide, Bay\u20105884, curcumin, valinomycin, aluminium, mercury, lead and copper. Diseases associated with accelerated eryptosis include sepsis, malaria, sickle\u2010cell anemia, \u03b2\u2010thalassemia, glucose\u20106\u2010phosphate dehydrogenase (G6PD)\u2010deficiency, phosphate depletion, iron deficiency, hemolytic uremic syndrome and Wilsons disease. Eryptosis may be inhibited by erythropoietin, adenosine, catecholamines, nitric oxide (NO) and activation of G\u2010kinase. Most triggers of eryptosis except oxidative stress are effective without activation of caspases. Their signalling involves formation of prostaglandin E<jats:sub>2<\/jats:sub> with subsequent activation of cation channels and Ca<jats:sup>2+<\/jats:sup> entry and\/or release of platelet activating factor (PAF) with subsequent activation of sphingomyelinase and formation of ceramide. Ca<jats:sup>2+<\/jats:sup> and ceramide stimulate scrambling of the cell membrane. Ca<jats:sup>2+<\/jats:sup> further activates Ca<jats:sup>2+<\/jats:sup>\u2010sensitive K<jats:sup>+<\/jats:sup> channels leading to cellular KCl loss and cell shrinkage and stimulates the protease calpain resulting in degradation of the cytoskeleton. Eryptosis allows defective erythrocytes to escape hemolysis. On the other hand, excessive eryptosis favours the development of anemia. 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