In response to binding of the TSHR-autoantibodies (TRAb) to the TSHR in OF’s, the TSHR and IGF-1R form a complex and thereby crosstalk (12, 13), one central pathogenetic factor contributing to TED progression and development of typical symptoms, such as exophthalmos, double vision, dry eyes and in serious cases compressive optic neuropathy (14). This evidence concerns the gene TSHR and Keratoconjunctivitis sicca.