Patients that have mutations in their potassium channel, improved their glucose levels with sulfonylurea regimen and glibenclamide showed successful results in managing glucose levels as well. A 2006 study showed that 90% of patients with a KCNJ11 mutation were able to successfully transition to sulfonylurea therapy. See also
Type 1 Diabetes
Type 2 Diabetes

References
Yorifuji, T; Kurokawa, K; Mamada, M; Imai, T; Kawai, M; Nishi, Y; Shishido, S; Hasegawa, Y; Nakahata, T (Jun 2004). "Neonatal diabetes mellitus and neonatal polycystic, dysplastic kidneys: Phenotypically discordant recurrence of a mutation in the hepatocyte nuclear factor-1beta gene due to germline mosaicism". The Journal of Clinical Endocrinology and Metabolism. 89 (6): 2905–8. doi:10.1210/jc.2003-031828. PMID 15181075. Edghill, EL; Bingham, C; Slingerland, AS; Minton, JA; Noordam, C; Ellard, S; Hattersley, AT (Dec 2006). "Hepatocyte nuclear factor-1 beta mutations cause neonatal diabetes and intrauterine growth retardation: support for a critical role of HNF-1beta in human pancreatic development". Diabetic Medicine. 23 (12): 1301–6. doi:10.1111/j.1464-5491.2006.01999.x. PMID 17116179. Works cited
Atkinson MA, Mcgill DE, Dassau E, Laffel L (2020). "Type 1 Diabetes Mellitus". In Melmed S, Auchus RJ, Goldfine AB, Koeng RJ, Rosen CJ (eds.). Williams Textbook of Endocrinology (14 ed.). Elsevier. pp. 1403–1437. De Franco E (December 2021). "Neonatal diabetes caused by disrupted pancreatic and β-cell development". Diabet Med. 38 (12): e14728. doi:10.1111/dme.14728. PMID 34665882. Garg M, Devaskar SU (2020). "Disorders of Carbohydrate Metabolism in the Neonate". In Martin RJ, Fanaroff AA, Walsh MC (eds.). Fanaroff and Martins Neonatal-Perinatal Medicine (11 ed.). Elsevier. pp. 1584–1610. ISBN 9780323567114. Katugampola H, Gevers EF, Dattani MT (2020). "Endocrinology of Fetal Development".
The previously listed genetic mechanisms result in twice the normal amount of these two genes and cause chromosome 6q24 TNDM. ZFP57 Gene
Third, mothers hypomethylation defects (a genetic defect that stops the allele from getting  a methyl group, which would inhibit transcription) can occur from an isolated genomic imprinting or occur as a defect called, "hypomethylation imprinted loci" (HIL). HIL is defined as the loss of a methyl group in the 5-methylcytosine nucleotide at a fixed position on a chromosome. Homozygous ( having two of the same alleles) or heterozygous (defined as having one each of two different alleles) ZFP57 pathogenic variant make up almost half of TNDM-HIL, but the other causes of HIL are unknown.Moreover, half of TNDM patients that contain chromosome 6q24-related TNDM experiencing re-occurrence of diabetes during their childhood or young adulthood. The onset of insulin resistance and increased insulin requirements are associated with puberty and pregnancy initiating the relapse of diabetes. In the event of remission, individuals do not show symptoms or impairment Beta-cell function in the fasting state. Insulin secretory response to intravenous glucose loading might be abnormal in those destined to have a relapse of diabetes. TNDM caused by 6q24 genomic defects are always associated with IGUR. Other contributing factors are umbilical hernia and enlarged tongue, which are present in 9 and 30% of patients with chromosome 6q24 related TNDM. Diagnosis
Diagnosis of neonatal diabetes is complicated by the fact that hyperglycemia is common in neonates – particularly in preterm infants, 25–75% of whom have hyperglycemia.