Revisiting the antagonistic pleiotropy theory of aging TOR-driven program and quasi-program

A half century ago, the antagonistic pleiotropy (AP) theory had solved a mystery of aging, by postulating genes beneficial early in life at the cost of aging. Recently it was argued however that there are very few clear-cut examples of antagonistically pleiotropic (AP) genes other than p53. In contrast, here I discuss that p53 is not a clear-cut example of AP genes but is rather an aging-suppressor (gerosuppressor). In contrast, clear-cut examples of AP genes are genes that encode the TO R (target of rapamycin) pathway. TO R itself is the ultimate example of AP gene because its deletion is lethal in embryogenesis. Early in life the TO R pathway drives developmental program, which persists later in life as an aimless quasi-program of aging and age-related diseases.