Major T-ALL subtypes are defined by aberrant oncogenic activation or chromosomal translocation events in genes coding for bHLH proteins (e.g., TAL1), LMO proteins (e.g., LMO1), homeobox proteins (e.g., TLX1, TLX3), or proto-oncogenes (e.g., c-MYB), while recurrent mutations target cell signalling pathways (e.g., NOTCH1, signal transduction), cell cycle regulatory mechanisms, and tumour suppressors (i.e. for inactivation) [52]. This evidence concerns the gene TLX3 and neoplasm.