Research reported that under the condition of dyslipidemia, TF and its downstream coagulation proteases could activate protease-activated receptors (PARs), then activate NF-κB or MAPK, ultimately exacerbating inflammation and fibrosis, leading to the progression of kidney damage (Oe & Takahashi, 2022). The gene discussed is NFKB1; the disease is Nephropathy.