As promoter substitution cannot be the common mechanism operating in these cases, we assume that non-IG rearrangements could either activate alternative internal promoter(s) of FOXP1 (http://www.humangenes.org) or lead to loss of negative regulatory elements, similar like activating rearrangements of LMO2 in T-ALL [49]. Here, LMO2 is linked to acute lymphoblastic leukemia.