KRAS and chronic obstructive pulmonary disease: GSEA results further demonstrated significant activation of inflammatory response, TNF-α signaling via NF-κB, and allograft rejection pathways in the COPD group, along with notable upregulation of KRAS signaling, mTORC1 signaling, epithelial–mesenchymal transition (EMT), and early and late estrogen response pathways (Figure 2F; Supplementary Table 4).