Similarly, fibroblasts isolated from the lungs of patients with IPF showed an increased invasive capacity compared to those of normal subjects, which were dependent on HAS2 and CD44 [91]; (2) the IPF myofibroblasts exhibiting an invasive phenotype showed a high production of HA associated with HAS2 upregulation, which was blocked by MK2 Inh (MMI-0100). This evidence concerns the gene HAS2 and idiopathic pulmonary fibrosis.