SP1 is a known regulator of proliferation, angiogenesis, and metastasis in various tumors, including osteosarcoma, gastric carcinoma, and glioblastoma.[15, 16, 17] Metabolic remodeling is a defining feature of advanced PDAC, driven primarily by mutant KRAS and characterized by enhanced glycolysis and macropinocytosis,[12, 18] whether SP1 coordinates metabolic remodeling in PanIN lesions remains unexplored – a gap this study addresses by integrating LCM‐based proteomics on human PanIN lesions and functional validation in transgenic mice. The gene discussed is SP1; the disease is glioblastoma.