Two liver‑fibrosis studies reported complementary advances: engineered CAR‑macrophage therapy reduced fibrosis in mouse models, offering a cell‑based anti‑fibrotic approach; separately, researchers identified NEK7’s role in stabilizing mitochondrial complex II (via SDHB) as a control point in fibrosis biology. The CAR‑macrophage data show that targeted reprogramming of innate immune cells can remodel fibrotic tissue and improve histologic endpoints in preclinical models—positioning cell therapy as a candidate for chronic liver disease. The NEK7‑SDHB mechanistic study links mitochondrial electron transport balance to fibrogenesis and identifies a kinase–respiratory chain axis that could yield small‑molecule or biologic targets. Together, the therapeutic and mechanistic reports suggest dual strategies—cell therapy for direct ECM remodeling and drug discovery targeting mitochondrial regulation—could be pursued in parallel for translational development.