This revealed that structural abnormalities, mainly rearrangements identified in T-ALL by karyotyping as a rare event [9,10,11,12,13,14,15,16,17,18,19], led to much overexpression of (1) basic helix-loop-helix (bHLH) transcription factor genes such as TAL1, TAL2, and LYL1; (2) LIM-only (LMO) domain genes such as LMO1 and LMO2; and (3) homeobox genes such as TLX1 (HOX11) and TLX3 (HOX11L2). Here, TLX3 is linked to acute lymphoblastic leukemia.