In sum, lung cancer pathogenesis reflects the integration of carcinogen-driven genomics with inflammation-shaped microenvironment, wherein IL-1β, IL-6, IL-8, TNF-α, and chemokines CCL2, CCL5, CXCL9 tune angiogenesis, myeloid skewing, T-cell response positioning, EMT, and checkpoint responsiveness, providing multiple mechanistic bridges to the cytokine–chemokine perturbations observed in acute and post-acute COVID-19 [45,46,47,48,49,50,52,82,83,84,85,90,91,92]. The gene discussed is IL1B; the disease is COVID-19.