SP1 and neoplasm: 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.