Of note, the monoclonal FLCs could also promote STAT1-dependent release of HMGB1, an injury-associated molecular pattern, and increase the expression of TLR2, TLR4, and TLR6 as well as downstream inflammatory responses, all of which were important underpinnings of the injury that might migrate into CKD (Upadhyay et al., 2020). The gene discussed is STAT1; the disease is chronic kidney disease.