In a mouse model of AP and in rat pancreatic acinar cells, transforming growth factor (TGF)-β was shown to upregulate miR-216a, which inhibited the expressions of PTEN and Smad7 and promoted AP via the PI3K/Akt and TGF-β feedback pathway (Zhang et al., 2015). The gene discussed is AKT1; the disease is alkaline phosphatase measurement.