Given the overlapping HLA class II susceptibility haplotypes in CD and T1D, and the growing evidence that tTG can modify beta cell antigens, it is reasonable to frame our discussion of when PTM occurs in T1D after our understanding of CD, where deamidation of gluten peptides by tTG results in preferential loading onto predisposing HLA-DQ molecules and the activation of pathologic CD4 T cells [34]. The gene discussed is CD4; the disease is type 1 diabetes mellitus.