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. Here, CDKN1A is linked to neoplasm.