Network analyses also revealed upregulated inflammatory responses and JNK signaling in KD-TN, including Tnf, Il-1b, Il-6, Ccl21, Mapk13, Tlr4, and Traf1. Notably, the elevated expression of Col1a1 and Anxa2 in KD-TN suggests enhanced ECM deposition that may initiate fibrosis, along with increased Nfkb2 and Krt8, which accelerate inflammation and cellular remodeling, key steps in the progression of steatosis to MASH. The gene discussed is CCL21; the disease is steatosis.