Indeed, SLE patient-derived blood neutrophils show increased REDD1 expression and basal autophagy, along with the formation of enhanced neutrophil extracellular traps (NETs), through a process known as NETosis, resulting in skin inflammation and renal fibrosis through the upregulation of tissue factor and IL-17A162. The gene discussed is DDIT4; the disease is systemic lupus erythematosus.