Because the anti-tumor activity of many conventional chemotherapeutic agents (e.g., doxorubicin, cisplatin, and etoposide) is mediated by p53 [45], [46], the p53-independent activation of p21 that was observed upon SF treatment could represent an alternative therapeutic approach for ALL patients that fail to respond to conventional agents targeting p53. The gene discussed is CDKN1A; the disease is acute lymphoblastic leukemia.