The PI3K/AKT pathway can activate downstream effectors including caspase-3, Bcl-2, VEGF, eNOS, NF-κB, and Nrf2, thereby participating in the processes of apoptosis, angiogenesis, inflammation, and oxidative stress in COPD pathogenesis (Figure 7). This evidence concerns the gene AKT1 and chronic obstructive pulmonary disease.