Ultimately, successful translation of BH3-targeted therapy will be defined by four key outcomes: (i) restoration of mitochondrial cooperativity in patients with post-venetoclax failure, reversing apoptotic resistance; (ii) minimization of platelet and cardiac toxicity through optimized drug chemistry and scheduling; (iii) enablement of time-limited, MRD-tethered treatment, reducing the burden of chronic therapy; and (iv) seamless integration with FLT3, IDH, and menin inhibitors, transforming BH3-centric therapy into a precision-tuned, relapse-resilient module applicable across AML subtypes. The gene discussed is IDH1; the disease is acute myeloid leukemia.