Unlike other anti-HER2 agents, T-Dxd’s unique clinical benefits in low HER2 BC may be associated with “indirect destruction” mechanisms due to the highly membrane-permeable payload, high drug–antibody ratio, and cleavable linker, primarily as a means of delivering antibody-conjugated drugs, rather than directly inhibiting HER2 dimerization or blocking downstream signaling. The gene discussed is ERBB2; the disease is breast cancer.