They also found that Krt8 and Krt18 were upregulated during ATII differentiation into ATI cells in vitro, and inhibition of TGFβ signaling attenuates Krt8/Krt18 upregulation [73], suggesting that TGFβ signaling might contribute to ATII transition cells/PEPs formation, thus recapitulating a failure of TGFβ signaling deactivation that may result in the persistence of ATII transition cells and PEPs in IPF [12, 73]. Here, KRT18 is linked to idiopathic pulmonary fibrosis.