Deletions in BCP-ALL result in a TAD more FLT3

The molecular consequences of coding mutations can often be predicted simply from their effect on a gene’s sequence. Noncoding mutations require more work. In this issue of Blood, Yang and colleagues¹ use 3D genomics to make an important contribution to the list of functional noncoding mutations in cancer. They show that microdeletions at 13q12.2 in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) eliminate the boundary of a topologically associated domain (TAD) at the FLT3 locus, which results in higher expression of FLT3, an important driver gene in acute leukemias.