Thus, it is conceivable that by lowering the overall F-actin content in MDA-MB-231 cells, Pfn1 depletion may create a similar cytoskeletal background and favour cell motility provided (1) other F-actin-dependent processes that are otherwise critical for normal cell motility, such as contractility, becomes less important, and (2) Pfn1 becomes dispensable in the case of tumour cells. The gene discussed is PFN1; the disease is neoplasm.