However, we found that mutation of K6 and K63 to arginine destabilized the Pin1 protein by inducing its poly-ubiquitination and degradation, which severely impaired the Pin1-mediated upregulation of SUMO1-sumoylation in GSCs (Supplementary Fig. 7a-d), indicating that sumoylation of Pin1 itself may play a unique regulatory role in cancer cells. This evidence concerns the gene PIN1 and cancer.