In summary, the tetrafunctional TriTECMs could consist of: i) dual tumour-targeting for increased tumour specificity by targeting EGFR and PD-L1, ii) engagement of T cells via CD3ε binding and bridging T cells in close proximity to tumour cells for tumour cell lysis, iii) increased T-cell-mediated cytotoxicity by blocking the PD-L1/PD-1 axis (checkpoint inhibitors), and iv) modulating cytokine storms or CRS by inhibiting the IL-6/IL-6R pathway by an anti-IL-6R scFv (Figure 6). The gene discussed is IL6; the disease is neoplasm.