In the previous study, the treatment of FGFC1 in an AKI mouse model improved the renal functional properties such as blood urea nitrogen, serum creatinine and fractional excretion of sodium, to minimize the renal tubule damage with excellent anti-oxidative and anti-inflammatory activities by inhibiting IL-1β, TNF-α, IL-6, and NF-κB (Figure 5) (Shibata et al., 2021). The gene discussed is IL1B; the disease is acute kidney injury.