Previous reports have established that IL-1α can act as a proinflammatory signal for kidney damage (Anders, 2016), where as Eotaxin and MIP-1α (CCL3) are potent chemokines that contribute to the recruitment of immune cells and promote AKI (Wada et al., 1999; Badenska et al., 2025; Chen et al., 2020). The gene discussed is IL1A; the disease is Nephropathy.