Thus, metabolic remodeling in PanIN lesions represents an early adaptive strategy to support biomass accumulation prior to angiogenesis and colonization, potentially collaborating with late‐stage metabolic adaptations that cope with hypoxia.[51] Correspondingly, pharmacological inhibition or genetic knockdown of SP1 or PFKFB4 effectively reversed aerobic glycolysis and suppressed tumor growth, demonstrating the potential therapeutic value of targeting these molecular targets. The gene discussed is PFKFB4; the disease is neoplasm.