Consistent with this approach, Marasco et al. reported B-cell activation responses to either CD40L, as T-cell-dependent stimulus, or CpG, as T-cell-independent stimulus of TLR9, in CVID patients as well as in patients with selective IgA deficiency using flow cytometry and checking upregulation of transcription factors for plasma cell differentiation (PRDM1, encoding BLIMP-1) as well as for class switching and somatic hypermutation (AID). Here, TLR9 is linked to selective IgA deficiency disease.