Furthermore, KD-TN elevated Col1a1 and Anxa2, promoting ECM depositions that may initiate fibrosis, alongside increased Nfkb2 and Krt8 expression, accelerating inflammation and apoptosis, key steps in the progression of steatosis to MASH (Supplemental Figure S1C, http://links.lww.com/HC9/C69, Figure 2G). The gene discussed is COL1A1; the disease is steatosis.