“… 4 , 5 During ageing, for instance, lipofuscin accumulation may be physiologically observed in the liver as well as in the central nervous system, at the level of which the occurrence of lipofuscin, lipofuscin-like lipopigments and ceroid may be also detected during oxidative stress, or as a response to given lysosomal storage diseases (Batten disease or neuronal ceroid lipofuscinosis ) 6 and to a number of physical and chemical noxae , such as radiation, cisplatin, lead (Pb) and mercury (methyl-Hg), under both natural and experimental disease conditions. 1 , 7-10 Moreover, lipofuscin and lipofuscin-like substances, which alongside with their well known AF properties 1 , 11 may be easily demonstrated in host cells by means of Schmorl and/or Sudan Black histochemical stains, 10 , 12 , 13 have been reported to increase in human mesenchymal stem cells subjected to oxidative stress, 14 while decreasing in murine embryonic stem cells undergoing differentiation, 15 a finding that might be of relevance also in relation to the recently described epithelial CSC-specific AF. 2 Beside what above, lipofuscin bodies may be observed in a number of additional pathologic conditions, both neoplastic and non-neoplastic, such as pancreatic tumours, non-choroidal melanomas, mammary gland carcinomas, pigmented eyelid cysts, retinal degenerative processes like age-related macular degeneration and brown bowel syndrome or intestinal lipofuscinosis.…”