The TSHR variant could act in several ways: (i) As a TSHR/TSAB binding protein to neutralise their effects and inhibit TSHR activation, as suggested in the current study; (ii) A potent autoantigen which could attract T cells to the orbit and contribute to the GO pathology; (iii) Since most GD/GO patients have a mixture of TSAB and TSHR-blocking antibodies (TBABs) which bind preferentially to the N’ and C’ termini of the LRR, respectively, the variant might bind TBAB, and thus, allow TSAB to predominate. This evidence concerns the gene TSHR and geroderma osteodysplastica.