We first focused on the transcription factor TAL1, whose dysregulation is a hallmark of approximately 40–60 percent of human T-ALL cases and often arises through chromosomal translocations (e.g., t (1;14) (p32;q11)) that lead to aberrant expression of TAL1 in T-cell progenitors [18]. Here, TAL1 is linked to acute lymphoblastic leukemia.