To gain insight into the feasibility of using the mutant HSV-1 as a therapy for ATRX-deficient tumors, we confirmed that mutant HSV-1 replicates ∼1000-fold more effectively in ATRX-deficient tumor cells than in ATRX-expressing fibroblast or healthy epithelial cells (Fig. 6A,B). This evidence concerns the gene ATRX and neoplasm.