UV radiation contributes to increased susceptibility to SLE by inducing inflammation and immune function change via upregulating multiple inflammatory mediators, interacting with the glutathione S-transferase Mu 1 (GSTM1) null genotype that clear reactive oxygen intermediate more slowly and therefore have more oxidative stress, and increasing the expression of nuclear autoantigens on the keratinocyte surface via triggering DNA damage [43, 45]. Here, GSTM1 is linked to systemic lupus erythematosus.