Their group suggests that circulating MPs that carry alarmin-like elements on their surface, like high mobility group box 1 (HMGB1+), play a role in the activation of non-classical monocytes in SLE patients and their migration to the kidney tissue, followed by the release of more MPs from those activated monocytes, intensifying this pathogenic loop [170]. This evidence concerns the gene HMGB1 and systemic lupus erythematosus.