A potential injury to the hippocampus has been postulated by the "glucocorticoid cascade hypothesis" as deriving from the life-long exposure to the stress glucocorticoid hormone. This hypothesis has been extensively resorted to in the search of a physio-pathological basis of the cognitive and behavioural impairments of old age, as well as for assigning to the hormone a not-irrelevant pathogenic role in brain degenerative diseases. Here I discuss the experimental evidences that have credited to stress a killing-licence, and pose, on the contrary, that the modest degrees of hypercortisolemia present in the above conditions could be interpreted as a beneficial occurrence.