TSHR and geroderma osteodysplastica: Moreover, we think it is the responsibility of the proponents of the hypothesis that stimulating IGF1RAbs are involved in GO pathogenesis to prove their hypothesis by isolating a monoclonal autoantibody from the blood of GO patients that binds to IGF1R, but not to TSHR, and activates IGF1Rs or TSHR/IGF1R crosstalk, or both.