It inhibited Rac1 and Cdc42 activity in cells at low‐micromolar concentrations.84 The same screening method identified AZA197 (46), which specifically inhibited Cdc42‐Dbs (RhoGEF) interactions by 61 % in vitro, although no IC50 value was calculated.85 It blocked Cdc42‐dependent migration and altered the cell morphology of cancer cells, whilst also suppressing colon cancer growth in vivo. Here, CDC42 is linked to cancer.