Other inflammatory and fibrotic pathways, such as MAPK/NF‐κB signaling, Wnt/β‐catenin cascade, PI3K/Akt signaling, or the hypoxia‐inducible factor‐1α (HIF‐1α) pathway, may act in concert with TGF‐β1/Smad3 to regulate fibrosis, adding to the complexity of fibrotic progression.[71, 72, 73, 74] Future studies exploring these complementary mechanisms will provide a more nuanced understanding of METTL3's role in renal fibrosis and its broader implications. The gene discussed is NFKB1; the disease is renal fibrosis.