The impaired interaction of the A-allele of AChE with miR-608 predicted weakened AChE suppression, resulting in elevated levels of free miR-608 molecules to suppress other targets with tight miR-608 binding sites, such as Cdc42 and IL6, which were already shown to be involved in IPF progression [13, 14]. The gene discussed is IL6; the disease is idiopathic pulmonary fibrosis.