Stemming from these observations, we drew a model for IL-1 production by CTX, which drives cancer cells into a cell cycle arrest, reminiscent of a pseudo-senescence state, which indicates a reversible senescence, employed by the cancer cells to protect themselves from drug toxicity, to finally re-enter into a proliferative state (rebound grow) through downregulation of p53 or p16 INK4A, expressing surviving, stemness marker or restoring nuclear and morphological structure (Chakradeo et al., 2015; Mastri et al., 2018; Saleh et al., 2018). Here, IL1B is linked to cancer.