The Human Stk11gene encodes the liver kinase B1 (LKB1) protein, which regulates metabolic signaling and determines susceptibility to stresses. In this study, we investigated whether the stk11 SNP rs9282860 (C>T) is associated with diabetic neuropathy in Type 2 diabetic patients. Four hundred type 2 patients were recruited and assessed 38 clinical parameters and SNP genotype. To assess interactions between the SNP genotype and stress factors such as HbA1c levels, we used a generalized linear model instead of comparing the neuropathy vs non-neuropathy group to determine the risk parameters. The number of nerves that showed slowed nerve conduction velocity (NCV) were influenced by the interaction of SNP alleles and HbA1c, serum cholesterol, and BUN. Surprisingly, serum cholesterol levels were negatively correlated with neuropathy. Bioinformatics analysis of diabetic peripheral nerve mRNA, most of which were from Schwann cells, revealed that a deficiency in LKB1function and cholesterol biosynthesis that affects myelin formation. This deficient can be compensated by transporter CD 36 expression which is also influenced by LKB1 expression. Since rs9282860's major allele (C) consists of a half CRE sequence, we tested the CRE involvement but not by linkage disequilibrium effect. We found that Prime Editing gene change CT to a full CRE sequence in reprogrammed human Schwann cells increased LKB1 mRNA and protein expression and prevented cellular senescence with increased NRF2 localization in the nucleus. As expected CD36 expression was also influenced by CRE genotype change. The study revealed a mechanistic relationship between stk11 rs9282860 and the development of diabetic neuropathy.