To summarize findings from these models: (1) similar immunization approaches yielded different outcomes in different mouse strains, indicating that genetic background plays an essential role in the development of TSAb; (2) free TSHR A subunits show significant advantages over full-length TSHR for inducing TSAbs, suggesting that the epitopes recognized for the generation of functional TRAbs are likely exposed in the free TSHR A subunit; and (3) Shimojo’s model has particularly emphasized that aberrant expression of MHC class II on non-APCs is a contributing factor to Graves’ disease. This evidence concerns the gene TSHR and Graves disease.