However, SARS-CoV-2 biology plausibly intersects with lung cancer pathways via ACE2/RAS, autophagy/lysosomal stress, inflammasomes, and immune checkpoint circuits, with IL-1β, IL-6, IL-8, IL-17, TNF-α, CXCL9, CCL2, and CCL5 as shared effectors shaping both acute COVID-19 and lung tumor microenvironments [6,7,8,18,33,67,73]. The gene discussed is IL1B; the disease is COVID-19.