It has been 50 years since cellular senescence was first described in human diploid fibroblasts (HDFs), yet its mechanism as well as its physiological and clinical implications are still not fully appreciated. Recent progress suggests that cellular senescence is a collective phenotype, composed of complex networks of effector programs. The balance and quality within the effector network varies depending on the cell type, the nature of the stress as well as the context. Therefore, understanding each of these effectors in the context of the whole network will be necessary in order to fully understand senescence as a whole. Furthermore, searching for new effector programs of senescence will help to define this heterogeneous and complex phenotype according to cellular contexts.