Childhood asthma and obesity are major public health problems, and their prevalence has markedly increased over the past several decades. There is extensive epidemiological, observational, and experimental evidence of an association between obesity and asthma. While in some children both diseases may simply coexist, there is growing awareness of a specific "obesity-related asthma" or "obese asthma" sub-phenotype, in which obesity increases asthma risk and morbidity-including worse asthma severity and control, more frequent exacerbations, reduced response to asthma medications, and poorer quality of life (1) .Much like obesity and asthma, "obese asthma" is a complex phenotype, underpinned by several contributing mechanisms. Obesity may lead to alterations in airway mechanics and lung function. Initial studies in adults described a restrictive deficit with symmetrically reduced FEV1 and FVC and lower lung volumes. However, some studies in children have described an obstructive pattern or airway dysanapsis (2) . Yet, others have described reductions in lung volumes like those seen in adults, suggesting that the consequences of obesity on airway mechanics may differ by age, severity, and duration. A recent study reported accumulation of adipose tissue within the airway walls of obese adults with asthma (3) , which would further explain some of the airflow obstruction seen in this phenotype.Obesity can lead to low-grade systemic inflammation that differs from the classic T2-high airway inflammation most frequently seen in pediatric asthma. Thus, inflammation in obese asthma may differ not just in quality (T2-low vs. T2-high) but also location (systemic vs. centered in the airway) (4) . Obesity has been associated with asthma in children without eosinophilic airway inflammation, but at the same time the coexistence of obesity and high FeNO is linked to worse asthma severity (5) . Systemic inflammation in obese asthma is mediated by adipokines such as leptin, and altered immune profiles including Th1 polarization, activation of monocytes, macrophages, and innate lymphoid cells (ILCs).Both obesity and asthma have high heritability. Mendelian randomization studies have reported that SNPs associated with obesity are associated with incident asthma (6) , and not vice versa.Recent genome-wide association studies (GWAS) have identified SNPs associated with late-onset asthma, non-atopic asthma, BMI, and waist-to-hip ratio (7) . Unlike the genetic code, epigenetic regulation and gene expression respond to the environment, and thus transcriptomic and epigenetic studies will allow us to evaluate the interaction between genetic susceptibility and socio-environmental factors that play an important role in obesity and asthma.Insulin resistance and metabolic dysregulation have also been implicated in obese asthma and resulting changes in lung function.Moreover, dietary changes in obesity may contribute to microbiome alterations, which could increase inflammation and contribute to asthma severity. Alternatively, it could be tha...