The possible explanations were as follows: (1) lncRNA DUXAP8 regulated the miR-29a/PIK3CA network and downstream PI3K-AKT pathway, as shown by subsequent molecule mechanism experiments, to modify cell proliferation, apoptosis, and Dox chemosensitivity in B-ALL, and (2) lncRNA DUXAP8 activated several key carcinogenetic pathways such as Wnt/β-actin, AKT/mTOR, and WTAP/Fak, to regulate these cell functions (34, 36, 37). Here, MTOR is linked to acute lymphoblastic leukemia.