The most common molecular hallmarks in T-PLL pathogenesis involve rearrangements of the T-cell leukemia 1 (TCL1) family gene loci of TCL1A or MTCP1. This juxtapositions them to T-cell receptor (TCR) gene enhancer elements, resulting in constitutive expression of these TCR signal amplifying oncogenes [5, 13, 14]. The gene discussed is TCL1A; the disease is T-cell prolymphocytic leukemia.