Interestingly, the expression of the NKG2D ligand, MICA, is upregulated on fibroblasts and the epithelial cells within the lung of IPF patients suggesting ligand concentrations, in addition to cytokine milieu, may play a role in directing NK cell function and the concerted modulation of NKT and γδ-T cells during progression of chronic lung disease (106). This evidence concerns the gene KLRK1 and idiopathic pulmonary fibrosis.