FN1 and neoplasm: Conversely, since TGF-β1 has been shown to be a major regulator for endogenous FN synthesis [276,277], platelet microaggregates may prompt secretion of TGF-β1 by platelets to further sustain E–M plasticity of CTCs, likely facilitating periFN assembly on tumor cells to make aggregation of CTCs with platelets stronger, rendering more resistance of CTCs to mechanical deformation in the circulation [278].