Since IPF MPCs are intrinsically fibrogenic under normoxic conditions, these findings prompted us to examine: (a) whether there were differences in lactate production between IPF and control MPCs under normoxic conditions and (b) whether hypoxia can enhance lactate production and release and, by operating through the lactate receptor GPR81, further augment IPF MPC fibrogenicity. This evidence concerns the gene HCAR1 and idiopathic pulmonary fibrosis.