## 3 Results
\begin{table}
\begin{tabular}{c c c c} \hline  & **GC (N = 11)** & **AG (N = 68)** & **AA (N = 93)** \\ \hline Mild asthma & 7/11 (63.6\%) & 35/68 (51.5\%) & 45/93 (48.4\%) \\ \hline Moderate-to-severe asthma & 4/11 (36.4\%) & 33/68 (48.5\%) & 48/93 (51.6\%) \\ \hline Age (years) & 61.9 \(\pm\) 11.0 & 54.4 \(\pm\) 14.6 \({}^{\lx@sectionsign}\) & 60.8 \(\pm\) 13.3 \\ \hline Gender (F) & 9/11 (81.8\%) & 41/68 (60.3\%) & 59/93 (66.4\%) \\ \hline BMI (kg/m\({}^{2}\)) & 29.9 \(\pm\) 7.7 & 26.0 \(\pm\) 4.7 \({}^{\star}\) & 26.7 \(\pm\) 5.1 \\ \hline Current smokers (\(\geq\)10 PY) & 2/11 (18.2\%) & 12/68 (17.6\%) & 28/93 (30.1\%) \\ \hline Former smokers (\(\geq\)10 PY) & 0/11 (0.0\%) & 1/68 (1.5\%) & 0/93 (0.0\%) \\ \hline Atopy & 5/11 (45.4\%) & 49/68 (72.1\%) \({}^{\lx@sectionsign}\) & 46/93 (49.5\%) \\ \hline Poly-sensitization & 5/5 (100\%) & 41/49 (83.7\%) & 35/46 (76.1\%) \\ \hline Asthma exacerbations/year & 0.9 \(\pm\) 1.3 & 1.2 \(\pm\) 1.3 & 1.4 \(\pm\) 1.6 \\ \hline FE Phenotype & 3/11 (27.3\%) & 20/68 (29.4\%) & 31/93 (33.3\%) \\ \hline Serum IgE (kU/L) & 273.3 \(\pm\) 524.6 & 361.9 \(\pm\) 519.4 \({}^{\lx@sectionsign}\) & 204.0 \(\pm\) 328.9 \\ \hline Serum IgE \textgreater{} 100 kV/L & 5/9 (55.6\%) & 41/57 (71.9\%) \({}^{\lx@sectionsign}\) & 32/69 (46.4\%) \\ \hline FeNO ppb & 31.2 \(\pm\) 20.0 & 37.3 \(\pm\) 27.3 & 40.8 \(\pm\) 27.9 \\ \hline FeNO \textgreater{} 30 ppb & 4/10 (40.0\%) & 26/60 (43.3\%) & 44/84 (52.4\%) \\ \hline Blood eosinophils (cells/uL) & 312.4 \(\pm\) 268.1 & 359.4 \(\pm\) 279.1 & 355.1 \(\pm\) 298.2 \\ \hline \end{tabular}
\end{table} 
Table 5: Descriptive statistics in the asthmatic population stratified for the A3669G polymorphism. Patients with the GG genotype of BclI had a higher percentage of patients with F\({}_{\rm E}\)NO > 30 ppb than patients with CC and CG genotypes and less percentage of patients with IgE > 100 kU/L than asthmatic patients with the CC genotype. No other relevant differences were observed between genotypes of Bcl (Table 4). Moreover, we analyzed the risk of carrying a specific genotype of Bcl for what concerns higher levels of IgE and F\({}_{\rm E}\)NO. The homozygote CC asthmatics had a major risk of having IgE > 100 kU/L (OR = 5.7; 95%CI = 1.6-20.7; \(p\) = 0.012) than homozygote GG asthmatics, while the BclI CC genotype (OR = 0.2, 95%CI = 0.04-0.7; \(p\) = 0.026) and BclI CG genotypes (OR = 0.2, 95%CI = 0.04-0.8; \(p\) = 0.031) are associated with a lower risk of having F\({}_{\rm E}\)NO levels more than 30 ppb than BclI GG genotype (Figure 1A). Examining the A3669G SNP, we observed that patients with the AG genotype were younger, allergic and had higher levels of serum total IgE more percentage of patients with IgE >100 kU/L compared to the AA genotype (\(p\) < 0.05). Furthermore, patients with AG genotypes were thinner than the GG genotype (\(p\) < 0.05) (Table 5). In order to identify whether distinct A3669G genotypes may predispose to specific asthma phenotypes, we performed odds ratio analyses for each factor characterizing our population. Patients with heterozygous AG had a greater probability to had atopic asthma (OR = 3.0; 95%CI = 1.6-5.9; \(p\) = 0.001) and had IgE >100 kU/L (OR = 3.0; 95%CI = 1.4-6.2; \(p\) = 0.006) than AA genotype (Figure 1A). No significant OR was observed when evaluating the possible association of A3669G SNP and obesity (BMI \(\geq\) 30 kg/m\({}^{2}\)). Finally, we observed that asthmatics carrying the BclI CC genotype had a greater risk of having IgE > 100 kU/L (OR = 2.2; 95%CI = 1.1-4.3; \(p\) = 0.036) than asthmatics carrying the A3669G AA genotype; moreover, patients with the A3669G AG genotype had a higher probability of being atopic (OR = 4.1; 95%CI = 1.4-11.1; \(p\) = 0.012) than asthmatics with GG BclI genotype (Figure 1B). Examining the lung function in the A3669G SNP, we found that asthmatics with the AA genotype had a lower post-bronchodilator FEV\({}_{1}\)/FVC ratio than the GG genotype (\(p\) < 0.05) and a higher RV/TLC ratio than the AG genotype (\(p\) < 0.05, Figure 2).