This suggests that the blocking of both IFNβ-dependent (for instance, with JAK inhibitors) and independent (with STING inhibitors) pathways may be the optimal therapeutic intervention to prevent excessive APOL1 expression in podocytes and possibly mitigate progression to LN in SLE patients carrying both APOL1 risk alleles. Here, IFNB1 is linked to systemic lupus erythematosus.