These therapies also represent a useful tool to optimize disease control, with a double positive effect on T1D: on one hand, reducing disease flares, whose inflammatory state causes hyperglycemia and glucose variability; on the other, limiting the prescription of corticosteroids, which are the staple of the treatment of the acute phase of some of these AIDs (IBDs, JIA, SLE, MS, nephrotic syndrome...), but have a deleterious effect on glucose metabolism, leading to hyperglycemia and reduction of insulin sensitivity. This evidence concerns the gene INS and nephrotic syndrome.