Replacement of the tyrosine kinase Syk with hyporesponsive Zap-70 in a Syk Zap-70 knock in mouse model resulted in impaired B cell selection, production of anti-insulin autoantibodies, and increased fasting blood glucose levels that may highlight impaired BCR signaling as a risk factor for T1D development [107]. This evidence concerns the gene BCR and type 1 diabetes mellitus.