Rac1 expression is increased in mouse and human pancreatic tumors, particularly in the stroma, and is generally a consequence of enhanced upstream inputs from receptor tyrosine kinases and phosphatidylinositol 3-kinases (PI3Ks) or of reduced Rac inactivation by GTPase-activating proteins (GAPs) (Heid et al, 2011). Here, RAC1 is linked to pancreatic neoplasm.