The active calystegine extract applied as a pre-treatment to the HuASCs enabled strong modulation of the overexpression of ATF6, PERK and IRE1-α ER sensors as well as CHOP pro-apoptotic effector protein in contrast to hyperglycaemic untreated cells (Figure 6), suggesting that calystegines counteract a hyperglycemia-induced loss of homeostasis in the ER. The gene discussed is ATF6; the disease is Hyperglycemia.