Similarly, WT1 overexpression in normal lung fibroblasts resulted in a marked upregulation of antiapoptotic genes, including BCL2, BCL2-L2, BCL-XL, and BCL3, mirroring the inverse effects observed in WT1 loss-of-function studies in IPF fibroblasts (Figure 5B and Figure 4A). Here, BCL2 is linked to idiopathic pulmonary fibrosis.