Rarely, the condition is caused by functional defects of β-cells (GCK), the destruction of β-cells due to apoptosis (EIF2AK3), autoimmune processes (FOXP3-IPEX syndrome), and defects of transcription factors (IPF1, GLIS-3, SLC19A, SLC2A2, NFT1B, PTFA1, GATA6, GATA4, and NEUROD1) [19,20]. This evidence concerns the gene SLC2A2 and immune dysregulation-polyendocrinopathy-enteropathy-X-linked syndrome.