On the other hand, all pairwise comparisons of the slow components among treatments (CNS SLE #4, anti-NR2A, anti-RPLP0) revealed a significant difference only between the two commercial autoantibodies (Kruskal Wallis, H2 = 12.414, p < .05; Dunn’s post-hoc tests, p < .05). The gene discussed is GRIN2A; the disease is systemic lupus erythematosus.