By interacting with TGFβ (79), tenascin-C sequesters TGFβ in an inactive state to prevent the induction of pro-dormancy cellular reprogramming and thereby enable proliferative signaling (83) (Figure 1E), although it is not clear if this is the central mechanism by which this ECM component contributes to aggressive NSCLC. Here, TNC is linked to non-small cell lung carcinoma.