However, the small difference between the percentages of myofibroblasts in IPF and control lung fibroblast cultures – together with the observation that COX-2-expressing fibroblasts were apparently indistinguishable from non-COX-2-expressing fibroblasts – suggests that the mechanisms involved in the down-regulation of COX-2 may also be present in IPF fibroblasts (α-SMA negative cells). Here, ACTA1 is linked to idiopathic pulmonary fibrosis.