Inhibition of Gal3 has demonstrated beneficial effects in myocardial fibrosis, idiopathic pulmonary fibrosis, non‐alcoholic steatohepatitis and CKD.[17] Genetic ablation of Gal3 significantly improves renal fibrosis in unilateral ureteral obstruction (UUO) mice, with macrophage‐derived Gal3 playing a pivotal role.[18] Additionally, kidney transplantation‐induced tubular atrophy and interstitial fibrosis are markedly alleviated in Gal3‐deficient mice.[19] Despite evidence highlighting the importance of Gal3 in tissue fibrosis, the specific molecular mechanisms remain incompletely understood. The gene discussed is LGALS3; the disease is Myocardial fibrosis.