Therefore, cytokine levels of SLE patients classified in the four combined IL-10/Atg5 genotypes suggested that those with normal autophagy function (Atg5 wild type), regardless of their IL-10 genotype, produced enough TNFα to counterbalance IL-10 levels, whereas Atg5 mutated patients were unable to control the genetically high IL-10 production (Table 5). This evidence concerns the gene IL10 and systemic lupus erythematosus.