Second, the mechanism of DPP-4i, which involves upregulating anti-apoptotic factors to enhance β-cell survival and prolonging the half-life of endogenous incretins (e.g., GLP-1 and GIP) to stimulate insulin secretion, is highly congruent with the core objective of preserving residual β-cell function in NEUROD1-deficient MODY6 (15, 16). This evidence concerns the gene NEUROD1 and maturity-onset diabetes of the young type 6.