Dear Editor,

Cohesin is a multiprotein complex that not only is essential for cell division but also has key roles in genome organization that underpin its gene regulatory function. Recurrent mutations of genes encoding cohesin subunits occur in myeloid malignancies at 10%–12% (Kon et al., 2013), and the frequency of cohesin mutation in Down syndrome-associated megakaryoblastic leukaemia is even higher (~50%) (Yoshida et al., 2013). Cohesin insufficiency reinforces stem cell programmes and impairs differentiation in haematopoietic stem cells (Mazumdar et al., 2015; Mullenders et al., 2015; Viny et al., 2015). The STAG2 subunit of cohesin is the most frequently mutated in myeloid malignancies (Kon et al., 2013). In contrast to other cohesin subunits, complete loss of STAG2 is tolerated due to partial compensation by STAG1. STAG2 and STAG1 have redundant roles in cell division (Benedetti et al., 2017; van der Lelij et al., 2017). However, cohesin-STAG1 and cohesin-STAG2 have non-redundant roles in facilitating 3D genome organization to delineate tissue-specific gene expression (Kojic et al., 2018).