We describe two new roles for Eps8: (1) when FAK is absent, Eps8 participates in a biochemical complex that controls the targeting of Src to autophagic structures, probably through effects on associated actin re-arrangements, and (2) when FAK is present (and co-upregulated with Eps8), Eps8 and FAK form a complex that is required for Src- and FAK-dependent cancer cell invasion in vitro. Here, SRC is linked to cancer.