In a simplified view, the proliferation of ErbB2-overexpressing tumour cells is driven predominantly by both ligand-independent homodimerization of ErbB2 (ref. 4) and heterodimerization with unliganded ErbB3 (ref. 3), whilst an autocrine ligand stimulation10 has been proposed to confer resistance against ErbB2 blockade via formation of ligand-containing heterodimers. The gene discussed is ERBB3; the disease is neoplasm.