The CXCL9–CXCR3 axis, which was upregulated in COVID-19, is thought to be involved in the recruitment of Th1 and CD8+ lymphocytes to sites of inflammation in COPD [45], with the subsequent immune-mediated lung damage occurring through the production of perforins and granzyme B [46]. The gene discussed is CXCR3; the disease is COVID-19.