Ongoing interactions between tumour cells and the tumour microenvironment throughout disease progression result in ECM fibre alignment, increased ECM deposition (collagens, laminins, fibronectin, proteoglycans etc.), increased crosslinking density and compositional changes within the ECM, which all contribute to increasing tissue stiffness as disease progresses (Fig. 1) [[4], [5], [6], [7], [8], [9], [10], [11], [12]]. This evidence concerns the gene FN1 and neoplasm.