Building on our findings, future studies could prioritize therapeutic strategies to modulate the Zc3h12c‐STAT1 axis—such as splice‐switching oligonucleotides correcting STAT1 isoform imbalances or small molecules enhancing Zc3h12c's RNase activity—to mitigate macrophage‐driven inflammation in kidney disease and beyond. This evidence concerns the gene STAT1 and kidney disorder.