Chromosomal rearrangements involving the ABL1 gene, leading to a BCR-ABL1 fusion 
gene, have been mainly associated with chronic myeloid leukemia and B-cell acute 
lymphoblastic leukemia (ALL). At present, six other genes have been shown to 
fuse to ABL1. The kinase domain of ABL1 is retained in all chimeric proteins 
that are also composed of the N-terminal part of the partner protein that often 
includes a coiled-coil or a helix-loop-helix domain. These latter domains allow 
oligomerization of the protein that is required for tyrosine kinase activation, 
cytoskeletal localization, and neoplastic transformation. Fusion genes that have 
a break in intron 1 or 2 (BCR-ABL1, ETV6-ABL1, ZMIZ1-ABL1, EML1-ABL1, and 
NUP214-ABL1) have transforming activity, although NUP214-ABL1 requires 
amplification to be efficient. The NUP214-ABL1 gene is the second most prevalent 
fusion gene involving ABL1 in malignant hemopathies, with a frequency of 5% in 
T-cell ALL. Both fusion genes (SFPQ-ABL1 and RCSD1-ABL1) characterized by a 
break in intron 4 of ABL1 are associated with B-cell ALL, as the chimeric 
proteins lacked the SH2 domain of ABL1. Screening for ABL1 chimeric genes could 
be performed in patients with ALL, more particularly in those with T-cell ALL 
because ABL1 modulates T-cell development and plays a role in cytoskeletal 
remodeling processes in T cells.