Our findings implicate mechanisms of T-cell escape in HPV + HNSCC, wherein high tumoral HPV-antigen load results in high expression of immune dysfunction genes on tumor cells (e.g., IDO-1) and dysfunction of HPV-specific CTLs (e.g., E7; E2-CTLs). HPV + HNSCCs expressing IDO-1 might similarly be driven by HPV-specific-CTL infiltration in response to high tumoral HPV-antigen load. The gene discussed is IDO1; the disease is neoplasm.