Collectively, acute COVID-19 generates a cytokine- and chemokine-rich environment (IL-1β, IL-6, IL-8, IL-17, TNF-α, CCL2, CCL5, CXCL9) that overlaps with lung-cancer-relevant circuits governing myeloid recruitment, T-cell positioning, angiogenesis, and tissue remodeling, setting the stage for the longer-term immune perturbations discussed next [42,43,44,45,46,47,48,49,50,51,52,115,116,117,118,119,120] (Figure 6). This evidence concerns the gene IL1B and COVID-19.