SLC26A4 and Hodgkins lymphoma: Our results suggest that specific disruption of the ability of SLC26A4 to interact with μ2 could be a target for a therapeutic approach with small molecules to increase SLC26A4 abundance at the cell surface and its function in patients with HL associated with pathogenic missense variants of SLC26A4 that are less abundant at the plasma membrane or able to reach the plasma membrane normally but are hypofunctional.