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We demonstrate this with a side-by-side comparison: one schematic generated by GPT-4o, the other created manually using BioRender and Adobe lllustrator. Both depict a complex hypothesis in pancreatic cancer: the ProA^high tumor subpopulation stabilizes ProB membrane localization to enhance glycolysis and lactate accumulation, activating Transferase C–mediated lactylation at lysine-x of histone Hx.x, which promotes ProD transcription and chemoresistance. Concurrently, ProA^high cells secrete TGF-β to induce CAF differentiation into myCAFs, reshaping the resistant tumor microenvironment. A biomimetic nanoparticle (PM-sGD@NPs) targeting ProA, combined with lactate metabolism intervention and gemcitabine, is proposed to reverse chemoresistance.