It has been found that 753B effectively eliminates AML cells and enhances the efficacy of chemotherapy by targeting senescent cells; this study also confirmed recent findings that standard chemotherapy with cytosine arabinose (Ara-C) induced cellular senescence (SnCs) in AML cells, manifested by increased cell size, the induction of senescence-associated β-galactosidase activity, the upregulation of cell cycle regulator proteins (p16, p21, p53), and the expression of the senescence-associated secretory phenotype factors (IL-6, IL-18, IL-1β), leading to chemoresistance in AML [89]. Here, IL18 is linked to acute myeloid leukemia.