Figure 1. Target of senolytics in the aging quasi-program. In post-mitotic quiescent cells in an organism, growth-promoting effectors such as mTOR drive conversion to senescence. Hyperfunctional senescent cells activate other cells (including cells in distant organs), rendering them also hyperfunctional, which eventually leads to organ damage. This process manifests as functional decline, a terminal event secondary to initial hyperfunction. Senolytics such as ABT263 or 737 kill hyperfunctional senescent cells, preventing damage to organs. Gerosuppressants such as rapamycin suppress geroconversion and may decrease hyperfunction of already senescent cells, thereby slowing disease progression (not shown here in scheme).