Our current SLE patient cohort further confirmed this blood basophil phenotype as evidenced by basopenia and overexpression of the activation marker CD203c, the chemokine receptor CXCR4, and the L-selectin CD62L, all of them being associated with disease activity (Supplementary Fig. 1d–j and Fig. 1g). The gene discussed is ENPP3; the disease is systemic lupus erythematosus.