Because we were unable to generate constructs lacking both DNA-binding domains, when we transplanted cells expressing each deletion construct into mice (Extended Data Fig. 14g), as expected, there was no significant difference in tumour growth rates (Extended Data Fig. 14h,i) or acetylated tubulin at the invasive front (Extended Data Fig. 14j), demonstrating that either HMGB2 DNA-binding domain is sufficient to maintain protein function. The gene discussed is HMGB2; the disease is neoplasm.