Scientists developed a molecular adapter called eCD16A/anti-CD3-BFP that transforms existing cancer antibodies into T cell-recruiting weapons. The bifunctional protein contains domains that simultaneously grab onto approved monoclonal antibodies like rituximab and cetuximab while activating nearby T cells to kill antibody-marked tumor cells. Testing across multiple cancer types showed the adapter effectively eliminated B cells, HER2-positive tumors, and EGFR-expressing cancers when paired with their respective targeting antibodies. This approach represents a significant advance in cancer immunotherapy engineering because it leverages the massive library of already-approved therapeutic antibodies rather than requiring entirely new drug development. The strategy could theoretically work with any IgG1 antibody, potentially expanding treatment options across dozens of cancer types. However, the research revealed that competing antibodies in patient blood can interfere with effectiveness, though higher doses or specially modified antibodies can overcome this limitation. The dual-mechanism approach—combining antibody targeting with T cell activation—may prove more durable than single-pathway therapies that often face resistance. If translated successfully to human trials, this adapter technology could represent a paradigm shift toward modular, mix-and-match cancer immunotherapy.