To verify the relevance of interface residues for receptor dimerization in vivo, we introduced either a mutation predicted to favour homodimer formation (Y764C, identified in both PCa and AIS patients) or the CAIS-associated mutation, P767A, in both EYFP- and ECFP-tagged AR-LBD fusions (Fig. 4c). The gene discussed is AR; the disease is posterior cortical atrophy.