Gain-of-function mutations in LTK are associated with the autoimmune disorder systemic lupus erythematosus, and it has been proposed that increased LTK activity, and therefore increased COPII-mediated ER export, allows plasma cells to cope better with the increased production and secretion of autoantibodies, thereby contributing to the autoimmune phenotype seen in lupus (Centonze et al., 2019; Li et al., 2004). Here, LTK is linked to systemic lupus erythematosus.