In chronic settings-including HBV infection, MASLD/MASH, and fibrosis/cirrhosis-we reveal a complex coexistence of functionally opposed subsets that concurrently drive pathology (e.g., <i>CD9</i> <sup>+</sup> <i>TREM2</i> <sup>+</sup> macrophages) and promote resolution (e.g., CD300E<sup>+</sup> macrophages). This evidence concerns the gene CD9 and Cirrhosis.