While the precise mechanisms of this process are still unclear, Fer-1, a small-molecule inhibitor, has been shown to reduce immune cell infiltration in models of acute kidney injury and decrease cytokine and chemokine expression levels (such as C-X-C-motif chemokine 2, interleukin 6, p65 subunit of NF-κB, interleukin 33, TNF-α, and monocyte chemotactic protein 1), suggesting that ferroptotic DAMPs can induce secondary immune cell activation and cytokine production. Here, NFKB1 is linked to acute kidney injury.