Cellular senescence is an autonomous tumor suppressor mechanism leading to a stable cell cycle arrest. Senescent cells are highly secretory driving a range of different functions through the senescence-associated secretory phenotype (SASP). Recent findings have suggested that the composition of the SASP is dynamically and spatially regulated and that the changing composition of the SASP can determine the beneficial and detrimental aspects of the senescence program, tipping the balance to either an immunosuppressive/pro-fibrotic environment or pro-inflammatory/fibrolytic state. Here we discuss the current understanding of the temporal and spatial regulation of the SASP and the novel finding of NOTCH signaling as a regulator of SASP composition.