Among them, the 3KLA-modified TDNs (3KLA-TDNs/DOX) exhibited the strongest mitochondria-targeting capacity, programmed apoptosis pathway activation, and tumor cytotoxicity by facilitating abundant release of cytochrome c; upregulating expression levels of caspase-3, caspase-9, p21, and p53; and downregulating the anti-apoptotic Bcl-2 protein expression and upregulating pro-apoptotic Bax. The gene discussed is CASP3; the disease is neoplasm.