We also analyzed the effect of TSP50 D206A mutant on the p110α-p85α interaction, and the results showed that p110α and p85α interacted more favorably in breast cancer cells with the TSP50 D206A mutation compared with the TSP50 wild-type breast cancer cells (Fig. 8G and H), further verifying the mechanism by which TSP50 activates PI3K/AKT signal. Here, PRSS50 is linked to breast carcinoma.