TAL1 and acute lymphoblastic leukemia: As a master TF in T‐ALL, overexpression of NOTCH inhibits p53‐mediated apoptosis.[7] Studies have shown that in T‐ALL cells, overexpression of TAL1 leads to elevated expression levels of several TFs, including RUNX family transcription factor 1 (RUNX1), MYB proto‐oncogene, transcription factor (MYB), ETS transcription factor ERG (ERG), and ETS proto‐oncogene 1, transcription factor (ETS1), thereby promoting leukemogenesis.[8, 9, 10, 11, 12, 13]