The survival advantage of TP53-deficient cells after BH3-mimetic drug exposure was not suppressed by the combination with either cytarabine or decitabine. (A) The in vitro growth of TP53 WT or TP53 KO MOLM-13 cells was monitored during continuous treatment with a suboptimal dose of cytarabine (100 nM AraC; left) or decitabine (1 µM DAC; right). Data are means ± SD of 4 independent experiments. (B) The growth of TP53 WT or TP53 KO MOLM-13 cells was monitored during continuous treatment with suboptimal doses of cytarabine (100 nM AraC; left panels) or decitabine (1 µM DAC; right panels) in combination with a suboptimal (IC₂₀) dose of venetoclax (100 nM). Data are means ± SD of 3 independent experiments. (C) The growth of TP53 WT or TP53 KO MOLM-13 cells treated continuously with a suboptimal dose of cytarabine (100 nM AraC) or decitabine (1 µM DAC) in combination with a suboptimal (IC₂₀) dose of the MCL-1i (10 nM; or control vehicle treated) was monitored. Data are means ± SD of 3 independent experiments. (D) The in vitro growth of TP53 WT or TP-53 KO MOLM-13 cells was monitored during continuous treatment with venetoclax (100 nM), MCL-1i (100 nM S63845) or combined venetoclax and S63845 (10 nM each drug) over 7 days. Data are means ± SD of 2 independent experiments.