The osteosarcoma study offered a precautionary perspective indicating that while HELLS level may reflect RB/E2F pathway inactivation, its upregulation may not always be synonymous with a critical role in tumor formation or tumor maintenance across all malignancies, and therefore should not be a warranted target for therapeutics against tumors in which HELLS overexpression is observed [7]. The gene discussed is HELLS; the disease is neoplasm.