In addition, since only constitutively active TAZ, which lacks the inhibition by the upstream inhibitor LATS1/2, can induce cancer stem cell and tumorigenic phenotype in lung epithelial cells, dysregulation of other components of the Hippo pathway may also play important role in lung tumorigenesis [4], TAZ-TEAD-Aldh1a1 may be a critical signaling axis in mediating CSC formation and tumorigenesis caused by dysregulation of other components of the pathway, and therefore a potential target for cancers with dysregulation of the Hippo pathway. Here, ALDH1A1 is linked to cancer.