To discern if there is a causal relationship between the above-observed inhibitory effect of Sal A treatment on PDF-elicited GSK3β hyperactivity and the beneficial effect of Sal A on oxidative injury and inflammation, primary cultures of PMC were employed and treated with medium containing hypertonic (4.25%) dextrose to model PDF-elicited peritoneal fibrosis in vitro (Figure 6). This evidence concerns the gene GSK3B and Peritoneal Fibrosis.