These results reveal that the protection against T1D exerted by the CDK11 hemideficiency in NOD mice is caused by a negative interference with cytokine (inflammation)-induced apoptosis, since, in the NOD/SCID strain, as expected, the apoptosis levels are negligible regardless of CDK11 expression levels, because there is no inflammation. The gene discussed is CDK19; the disease is type 1 diabetes mellitus.