Collectively, prior results and our new findings suggest that GPR‐81, LDHA, and LDHB were also abnormally expressed in IPF lung tissues, further supporting our concept that the alteration of LDHA/LDHB and lactate/GPR‐81‐mediated signaling may contribute to the pathobiology of IPF. Here, HCAR1 is linked to idiopathic pulmonary fibrosis.