Considering these findings along with the absence of polymorphisms within the miR-6891-5p gene and the observed significantly elevated expression of HLA-B and miR-6891-5p within B-LCLs from patients with selective IgA deficiency, our data suggest a disease model in which the accumulation of miR-6891-5p transcripts may play a role in the pathophysiology of the disease by attenuating expression of IgA. Here, HLA-B is linked to selective IgA deficiency disease.