Exogenous wild-type RanBP9 was interacted with endogenous TSSC3 to exert a tumor-suppressive effect, as indicated by reduced anchorage-independent growth and anoikis resistance, as well as decreased phosphorylations of both Src Tyr418 and Akt Ser473; however, these tumor-suppressive effects were attenuated by deletion of the SPRY domain of RanBP9 (Figures 5d and f; Supplementary Figure S8b). Here, AKT1 is linked to neoplasm.