Together, substantial evidence indicated that altered hepatokine (fetuin-A, SeP, and FGF21), adipokine (leptin, adiponectin, and RBP4), cytokines (IL-6 and TNF-α), EVs (miR-122), and gut-derived factors (SCFAs and TMAO) in NAFLD patients participated in the development of hypertension through inducing inflammation, IR, endothelial dysfunction, and RAAS and SNS activation. The gene discussed is SELENOP; the disease is metabolic dysfunction-associated steatotic liver disease.