To confirm that cancer cells often undergo plasticity in cell motility, the opposite transition has been also described: the group of Marshall demonstrated that A375 M2 melanoma cells move in a rounded, amoeboid manner on top of or through collagen matrices due to JAK1-dependent MLC2 phosphorylation, whereas silencing of JAK1 induces a reduction in the acto-myosin contractility and the acquisition of an elongated morphology [21]. This evidence concerns the gene JAK1 and melanoma.