In mouse models of MASH, LAMs are recruited via an oxidized low-density lipoprotein (oxLDL)–TREM2–rapamycin complex 2 (mTORC2) axis and contribute to the resolution of liver fibrosis in a TREM2 and peroxisome proliferator-activated receptors δ/γ (PPAR-δ/γ) dependent manner. Here, TREM2 is linked to metabolic dysfunction-associated steatohepatitis.