Silencing FMNL2 in gastric cancer and melanoma suppressed cancer cell migration.[16, 17, 18, 19] Previous work revealed that downstream of Rac1 activity, FMNL2 binds to components of the adherence junction complex at newly forming cell‐cell contact sites, where it drives the assembly of junctional actin.[4] In contrast to this pro‐epithelialization function of FMNL2, we also showed that PKCα‐dependent phosphorylation at a specific C‐terminal serine residue promotes trafficking of integrins, a necessary process in cancer cell invasion.[7]. This evidence concerns the gene FMNL2 and melanoma.