SOX9 and neoplasm: Forced upregulation of SOX9, obviating the need to downregulate PTF1a and MIST1, has also been shown to stimulate transdifferentiation of acinar cells into a ductal cell phenotype susceptible to KRAS-induced neoplasia [112], implicating SOX9 as a key functional effector of their downregulation in the genesis of human PDAC (Figure 4).