The breakpoint cluster region of AFF1/AF4 also showed DNase I sensitivity (Strick et al., 2006), so that the therapy/infant-related MLLbcr breaks and rearrangements could be due to increased accessibility of this translocation hotspot for nucleases such as topoisomerase II and Endonuclease G. No such features were described for the centromeric part of the MLLbcr (Figure 1B), suggesting that the mechanisms of MLL breakage leading to de novo AL are quite different from the ones in t-AL and infant ALL. The gene discussed is AFF1; the disease is axial length measurement.