As PDAC progresses, PRMT1 expression gradually increases. PRMT1 methylated two conserved arginine residues on HSP70, which then binds to BCL-2 mRNA through AU-rich elements (AREs) in its 3′-untranslated region (3′-UTR). This interaction stabilises BCL-2 mRNA, leading to increased BCL-2 protein expression. Consequently, cancer cells exhibit enhanced drug resistance and anti-apoptotic properties. The gene discussed is BCL2; the disease is cancer.