Initial studies of the BJAB B-cell line suggested the existence of a third BAFF receptor, since it bound high levels of BAFF although no or/low levels of TACI and BCMA were found. A novel BAFF receptor, BAFF-R, which was found to be specific for BAFF, was cloned from a BJAB library. The authors also generated a recombinant BAFF-R-Fc fusion protein, which inhibited BAFF binding to BJAB cells and inhibited BAFF-mediated co-stimulation of B-cell proliferation. BAFF-deficient mice have profound B-cell defects reminiscent of the A/WySnJ mouse strain, the authors examined BAFF-R expression in A/WySnJ mice. BAFF-R expressed in the A/WySnJ mice lacks exon 3, which encodes the intracellular signalling domain of BAFF-R; this defect presumably eradicates its function. Neither the TACI nor BCMA knockout mice have B-cell deficiencies similar to BAFF knockout mice, implicating BAFF-R as the major effector for BAFF-mediated B-cell survival. Additionally, APRIL and BAFF signalling through TACI and BCMA could not compensate for loss of BAFF-R, demonstrating its critical role in B-cell survival and homeostasis. BAFF-R and its deficiency in A/WySnJ have been reported by another group (see Additional information ), although they name the new receptor BLyS receptor 3.