1. Targeting Apoptosis in AML

2. The Pathogenesis of AML

3. Strategies to Combat AML

4. Mechanism of BCL-2 Inhibition in AML: “Apoptosis Hypothesis”

5. Cells Use the BCL-2 Family of Proteins to Decide Whether to Die or to Survive

6. Venetoclax Is a Potent, Selective Inhibitor of BCL-2

7. Mechanism of BCL-2 Inhibition in AML: “Leukemia Stem Cell Hypothesis”

8. In Vivo Evidence of Decreased OXPHOS and Leukemia Stem Cell Targeting

9. Mechanism of BCL-2 Inhibition in AML: “Leukemia Stem Cell Hypothesis”

10. Mechanism of BCL-2 Inhibition in AML: “Leukemia Stem Cell Hypothesis” (Cont.)

11. Venetoclax + HMAs in Elderly Patients With Untreated AML: Study Design

12. Response Rates With Venetoclax + Baseline Therapy

13. Response Rates With Venetoclax + Baseline Therapy: Subgroup Analysis

14. Response Duration With Venetoclax + Backbone Therapy

15. OS With Venetoclax + Backbone Therapy

16. Frequencies of Common Recurrent Gene Mutations in Adults With AML

17. IDH1/2 and FLT3 Mutations in AML

18. BCL-2 Inhibition in Combination With Other Agents

19. Venetoclax With LDAC in Treatment-Naive, Elderly Patients With AML Unfit for Intensive CT: Efficacy

20. Venetoclax With LDAC in Treatment-Naive, Elderly Patients With AML Unfit for Intensive CT: Efficacy (Cont.)

21. Novel Combinations in Progress or Development: Front-Line Setting

22. Novel Combinations in Progress or Development: Relapsed Setting

23. Clinical Outcomes From BCL-2 Inhibition

24. Clinical Applications of BCL-2 Inhibition

25. Conclusions

26. Abbreviations

27. Abbreviations (cont)