Objective: To describe role of precision medicine in genetically diagnosed Maturity Onset Diabetes of Young (MODY) Methods: Three individuals diagnosed as MODY on basis of clinical and genetic criteria. Anti-diabetic drugs were selected according to presumed molecular pathway defect in diabetes causation Results: All subjects had BMI < 25 kg/m2, diabetes onset age < 25 years, strong family history of type 2 diabetes, Anti- GAD 65 and Anti-insulin antibodies were absent. There were no other comorbid conditions. Remarkable response to particular class of anti-diabetic drugs observed. Case 1: 38 yr male (DM since 12 years) was found to have ABCC8 exon 61 defect.Previouly uncontrolled on (Glimeperide 4 mg OD + Metformin 1,000 mg OD + Linagliptin 5 mgOD) responded to Repaglinide 2 mg OD. Likely molecular mechanism: B site SURI receptor mutation could impede response to glimepiride but not repaglinide Case 2: 33 yr female (DM since 17 years) found to have INS exon2 227 G >A defect.Previously uncontrolled on Premix Insulin 24 U before meals responded well to Sitagliptin 50 mg + Metformin 500 mg OD.Hypothesis: Defect in unfolded protein response (UPR) leading to incretin defect. Case 3: 24 yr male (DM since 3 years) found to have PPARG exon 11 C>T defect. Previously uncontrolled on (Glimeperide 2 mg OD+ Vildagliptin 50 mg BD+ Metformin 1,000 mg BD) responded to Saroglitazar 4 mg OD + Dapagliflozin 10 mg OD.Hypothesis: PPAR gamma receptor structural change may lead to better response to dual PPAR alpha and gamma agonist Conclusion: MODY cases described above provide novel insight for therapeutically targeting molecular pathways in diabetes mellitus. Further intervention studies are needed in genetically diagnosed MODY subjects to tailor anti-diabetic drugs according to molecular defect