Pancreatic ductal adenocarcinoma (PDAC) constitutes 90% of all pancreatic malignancies and is characterised by extensive desmoplasia and early metastasis. The risk factors for PDAC include a family history of the disease, cigarette smoking, chronic pancreatitis, obesity and diabetes mellitus (1,2). PDAC most commonly occurs in the 60 to 80 year age group, and its incidence is 50% higher in men than in women and (1) genetic mutations such as BRCA2, CDKN2A, STK11, PRSS1, SPINK1, CFTR, PALB2 and ATM increase the risk for PDAC (3), patients with chronic pancreatitis have a 15 fold increased risk of developing PDAC (4), cigarette smoking increases the risk of PDAC by 75% even up to 10 years after cessation of smoking and (5) diabetes mellitus increases the risk by 30% up to 20 years after diagnosis (6). Obesity and high body mass index are positively correlated with the risk of developing PDAC (7). One meta-analysis showed a 19% increase in risk of developing PDAC in obese individuals (BMI ≥30 kg/m 2) compared to normal participants (BMI 22 kg/m 2) (8). The genetic mutational landscape of PDAC involves the alteration of 69 genes which affect 12 core signalling pathways (9). Both oncogenes and tumour suppressor genes are mutated of which the major genes involved in PDAC are the oncogene Kristen Rat Sarcoma Virus (KRAS), and three tumour suppressor genes-TP53, CDKN2A and SMAD4. KRAS is the earliest mutation seen in low-grade pancreatic