SMR analysis revealed that MFSD10, TET2, and HTT did not exhibit significant causal effects on COPD in their corresponding tissues (PSMR−FDR > 0.05), nor did they share the same genetic signals with COPD in colocalization analysis (PP.H4 < 50%), suggesting that changes in their expression may not directly contribute to COPD pathogenesis (Supplementary Material 1, S6 and S7). The gene discussed is TET2; the disease is chronic obstructive pulmonary disease.