TIMP1 and cancer: Recent evidence in this new field demonstrated that mechanical tension, induced by hypotonic swelling or biaxial stretch, stimulates ER‐Exit Sites (ERES) number and enhances the ER to Golgi transport of Mannosidase II via Rac1.[25] Similarly, the matrix stiffness, commonly altered in fibrotic diseases and known to regulate several hallmarks of cancer,[26, 27, 28] has been demonstrated to increase PM tension, a process promoting Tissue Inhibitor of Metalloproteinases 1 (TIMP1) exocytosis via Caveolin1 and Dynamin2.[29]