Targeting key components of tumor suppressors, such as phosphatase and tensin homolog (PTEN), tuberous sclerosis 1/2 (TSC1/2), neurofibromin 1/2 (NF1/2), or oncogenic mutations in KRAS, PIK3CA, or AKT, may represent an effective treatment to kill acute myeloid leukemia and leukemia stem cells, according to growing evidence (Grabiner et al. 2014). The gene discussed is AKT1; the disease is neoplasm.