However, loss of CTCF binding did result in clear alterations to the chromatin loops involving the posterior HOXA genes, including HOXA9 and HOXA10. Specifically, long-range loops were diminished, and were replaced by compensatory interactions with regions of the SKAP2 gene, which also appear to directly interact with active HOXA genes in primary AML samples with the NPM1c mutation. The gene discussed is HOXA10; the disease is acute myeloid leukemia.