Two studies, including one by our group, have recently reported that coding variants in TNFRSF13B, which encodes TACI (transmembrane activator and CAML interactor), are associated with primary immunodeficiencies in humans1, 2. In our original study1, we reported heterozygous TNFRSF13B coding variants in 4 of 19 individuals with common variable immunodeficiency (CVID). Since then, we have collected sequencing data on 106 individuals with CVID and 62 controls. The genotype frequencies for the coding variants we observed are given in Table 1. We found a significant association between CVID and the heterozygous coding variants C104R (5/212 versus 0/124; P= 0.030 by χ2 test) and A181E (4/212 versus 0/124; P= 0.052). We also observed five heterozygous variants (L69fsX11, Gly76fsX3, R72H, L171R and R202H) in individuals with CVID but not in controls, but the differences were not statistically significant. One of these variants, R72H, has been previously reported in healthy controls2. Finally, we observed six variants in both affected individuals and controls. Two of these result in amino acid substitutions (V220A and P251L) and have been described previously1–3.