Aside from the overexpression of TEs in AT2 IPF cells, we also find that the dysregulation of TEs is likely further facilitated by the decreased expression of the autophagy gene CALCOCO2 (NDP52), which is known to be crucial receptor for the detection and removal of at least one TE RNA family (L1). This evidence concerns the gene CALCOCO2 and idiopathic pulmonary fibrosis.