Interestingly, although the ERK3 kinase activity was necessary for the formation of actin‐rich protrusions in mammalian cells (e.g. primary mammalian epithelial HMEC, or cancer‐derived MDA‐MB‐231 cells) and ERK3 directly bound to the ARP2/3 complex, phosphorylating ARP3 at Ser‐418, the kinase activity of ERK3 was dispensable for the F‐actin accumulation in HMEC cells. This evidence concerns the gene MAPK6 and cancer.