The absence of B cells (due to the homozygous knockin of the Mb1‐cre allele) or T cells (due to the loss of CD3ε) did not change the kinetics or severity of arthritis and heart disease in BPSM1 mice.3 In contrast, loss of B cells prevented the development of TLO in both the lungs and the bone marrow of BPSM1m/+Mb1‐creKI/KI mice (Figure 2a), whereas lymphocyte follicles were still present in both these locations in T cell‐deficient animals (in BPSM1m/+CD3ε−/− mice) (Figure 2b). The gene discussed is CD3E; the disease is heart disorder.