Sun et al. observed that exosomes with macrophage-derived angiotensin II type 1 receptor (AT1R) activate the renin–angiotensin system (RAS) and the TGF-β-Smad2/3 pathway through a shift to the Ang II–AT1R axis, promoting collagen synthesis and mediating BLM-induced lung fibrosis [90]. The gene discussed is TGFB1; the disease is pulmonary fibrosis.