Type 2 diabetes (T2D) is known as a risk factor for pancreatic cancer (PC). Various genetic and environmental factors cause both these global chronic diseases. So, the mechanisms which define their relationships are complex and poorly understood. Recent studies implicated that metabolic abnormalities, including hyperglycemia and hyperinsulinemia, could lead to cell damage responses, cell transformation, and increased cancer risk. Hence, these kinds of abnormalities following molecular events could be essential to develop our understanding of this complicated link. Among different molecular events, focusing on shared signaling pathways including metabolic (PI3K/Akt/mTOR) and mitogenic (MAPK) pathways in addition to regulatory mechanisms of gene expression like involved non-coding RNAs (miRNAs, circRNAs, and lncRNAs) could be considered as powerful tools to describe this association. A better understanding of molecular mechanisms involved in developing T2D and PC would help us find a new research era for developing therapeutic and preventive strategies. For this purpose, in this review, we focused on the shared molecular events resulting in T2D and PC. First, a comprehensive literature review was performed to determine similar molecular pathways and non-coding RNAs; then, the final results were discussed in more detail.