In addition, γ-H2AX (a DNA damage marker), the cleavage form of caspase-3 (an apoptosis maker), and α-SMA (a fibrosis marker) were significantly increased in the MD tissue (Fig. 2b), implying that an increase in YAP1 may be related to DNA damage, apoptosis, and fibrosis in vivo. This evidence concerns the gene H2AX and Menkes disease.