Recent studies in Type 1 Diabetes (T1D) research have focused on genetic factors and immune responses that contribute to the disease. One significant finding is the role of insulin mRNA decay in modulating the risk of T1D, particularly through the unfolded protein response that activates inositol-requiring enzyme 1α (IRE1α). This mechanism appears to be influenced by specific genetic variations, such as the SNP rs3842752, which may provide genetic protection against T1D by affecting insulin mRNA stability (ref: van Tienhoven doi.org/10.1016/j.cell.2025.02.018/). Additionally, the development of a simple whole-blood assay called BASTA has enabled the measurement of T cell responses to β cell antigens, which are crucial for understanding the autoimmune processes in T1D. This assay could facilitate earlier detection of β cell autoimmunity compared to existing autoantibody tests (ref: Lacorcia doi.org/10.1126/scitranslmed.adt2124/). Furthermore, research into T cell receptor precision editing has shown promise in addressing celiac disease, which shares genetic predispositions with T1D, highlighting the interconnectedness of autoimmune disorders (ref: Porret doi.org/10.1126/scitranslmed.adr8941/).