PDOs also enable functional dissection of senescence–immunity crosstalk: in gastric cancer, AURK inhibitor-treated organoids exhibit canonical senescence (enhanced SA-β-Gal, multinucleation) and secrete high CCL2; in PDO–macrophage co-culture, the CCL2–CCR2 axis recruits and polarizes M2 macrophages, dampening innate tumor cell clearance. Here, CCL2 is linked to neoplasm.