Asthma is a very heterogeneous disease, with two major asthma phenotypes, the allergic and the late onset asthma, differentiated by the triggers, the cellular dominance, the Th1/Th2 inflammation pattern and the local and serological markers. As there were many overlapping biological markers between these two phenotypes, different types of tentative classification followed. A clinical one makes a difference between the predominant eosinophilic one (with better response to glucocorticoid) and the predominant neutrophilic one with more severe evolution and low rate of therapeutical improvement. Another approach was based on cluster analysis of asthma characteristics (onset, atopic status, and body mass index (BMI)), sensitivity to methacholine test, peak flow variability, bronchodilatation response, postbronchodilator level of FEV1, sputum eosinophil and neutrophil count, FeNO test, clinical symptom scores, treatment scheme to control symptoms, exacerbations, and severity. Emerging data suggest a distinct late onset obese-asthma phenotype, with a specific pathophysiology, comorbidities, and clinical evolution. This chapter reviews the main characteristics of this phenotype: the specific lung function impairment, the underlying inflammation, the adipokine profile, the comorbidities and the therapeutical approach. The mutual influence between obesity and asthma will be illustrated, whenever scientific data are available.