By developing the UMAI construct on the basis of human ATF4 gene and introducing the construct into HeLa or NIH3T3, we were able to confirm that luciferase activity increased markedly in response to deprivation of a specific amino acid (Leu) as well as to treatments with poly(I)poly(C) nucleotide (pIC), which mimics virus infection; tunicamycin (Tun), an endoplasmic reticulum (ER) stress inducer; and sodium arsenite (ASN), an oxidative stress inducer (Fig. 3a). This evidence concerns the gene ATF4 and viral infectious disease.