Since the sustained hyper-expression of MHC-I is a defining feature of islet cells in type 1 diabetes (Richardson et al. 2016, Marroqui et al. 2017, Wyatt et al. 2019) (and occurs in EndoC-βH1 cells following exposure to type I, II or III interferons) (Marroqui et al. 2017, Colli et al. 2020), it is tempting to hypothesise that this is mediated by the long-term increase in unphosphorylated STAT1/2 seen following exposure of the cells to each IFN isoform. Here, SGCG is linked to type 1 diabetes mellitus.