While clinically effective in hematological malignancies, their therapeutic limitations in solid tumors motivate our proposal: Pharmacokinetically optimized dual PAK1/HDAC IIb inhibitors may overcome TNBC heterogeneity through multi-mechanistic modulation of energy metabolism pathways, PAK1/HDAC10-mediated tumor microenvironment dynamics, and their functional cross-talk. The gene discussed is PAK1; the disease is hematologic disorder.