Abstract: Programmed cell death protein 1/programmed death-ligand 1 (PD-1/PD-L1) immune checkpoint blockade can relieve T-cell suppression; however, its therapeutic efficacy remains limited by factors such as insufficient costimulatory signaling. Because 4-1BB costimulation promotes T-cell activation and effector function, simultaneous modulation of these two pathways may enhance antitumor immunity. In this study, human ferritin heavy chain (FTH1) nanocages were engineered to co-display a PD-L1-blocking peptide (PDL1b) and a tandem 4-1BB agonistic peptide (2×4-1BB). Functional evaluation showed that the nanocage displaying a single copy of the 4-1BB agonistic peptide, FTN-1×4-1BB, elicited no appreciable costimulatory activity, whereas the tandem-peptide nanocage, FTN-2×4-1BB, significantly enhanced Ifng expression in anti-CD3-stimulated primary mouse splenocytes. FTH1-PDL1b and FTH1-2×4-1BB were subsequently co-assembled through pH-controlled disassembly and reassembly at a feed molar ratio of 3:1, yielding the dual-targeting nanocage FTN-Dual. In vitro, FTN-Dual exhibited enhanced binding to IFN-γ-pretreated CT26 cells and increased the proportion of IFN-γ⁺CD8⁺ T cells from 4.65% to 9.34%, demonstrating combined immunomodulatory activity. In a CT26 tumor-bearing mouse model, FTN-Dual achieved a tumor inhibition rate of 67%, prolonged median survival from 48 to 60 days, and reduced the proportion of CD8⁺ T cells with an exhausted phenotype within tumors from 29.4% to 12.7%. No evident abnormalities were detected in the liver function parameters or histopathological examinations of major organs assessed in this study. Collectively, FTN-Dual enhanced T-cell-associated antitumor immunity, inhibited tumor growth, and prolonged survival in tumor-bearing mice, providing a new strategy for the development of a non-antibody-based, dual-targeting nanoimmunotherapy platform.