In the Alzheimer’s disease mice model based study, it was found that when autophagy is genetically hyperactivated by knocking-ina gene-point mutation (Becn1F121A) in the autophagy essential gene (Beclin 1/Becn 1), a significant decrease in amyloid accumulation is observed and there is a prevention of cognitive decline along with restoring the survival of AD mice.This happens because the F121A point mutation induced in Becn 1 significantly decreases the interaction of BECN 1 with its inhibitor BCL2, leading to constitutively active autophagy even in non-autophagy inducing conditions [124]. This evidence concerns the gene BCL2 and Alzheimer disease.