Indeed, the overexpression of HIPK2-CT in kidney tubular cells was sufficient to attenuate the expression of inflammatory cytokines and macrophage infiltration in the kidneys of mice with unilateral ureteral obstruction (UUO) and LPS-induced acute kidney injury (AKI), demonstrating that HIPK2-CT can be further exploited as a therapeutic approach to restrain renal inflammation in vivo. The gene discussed is HIPK2; the disease is inflammation.