#Respiratory #inflammation spans a spectrum of upper and lower airway diseases, asthma, chronic rhinosinusitis, allergic and non-allergic rhinitis, and COPD, unified by overlapping type 2 and non-type 2 inflammatory mechanisms. Biologic and small-molecule therapies targeting IL-4/IL-13, IL-5, IgE, and corticosteroid-responsive pathways have reshaped management across these conditions, shifting the therapeutic aim from symptom control toward sustained remission. Substantial heterogeneity nonetheless persists in inflammatory endotype, airway remodeling, and treatment response. This complexity is driving growing interest in transcriptomic, metabolomic, and cellular signatures capable of endotyping respiratory inflammation across the airways. In this issue, Roth-Walter et al. present a EAACI position paper discussing small-molecule drugs and RNA-based therapeutics as an emerging complement to biologics in precision medicine for chronic inflammatory diseases. Scheire and Lourijsen et al. present an EAACI Task Force meta-analysis showing that cumulative systemic glucocorticosteroid doses between 500 mg and 1 g prednisolone-equivalent significantly raise the risk of adverse effects in patients with upper airway disease and asthma. Gunaydin et al. review the evidence and predictors behind asthma remission as an achievable treatment goal. Nguyen et al. discuss the growing use of artificial intelligence in allergy, asthma, and immunology, including its association with environmental exposure data. Virchow and Bertels et al. present a EUFOREA consensus aiming to establish practical guidance for inducing and maintaining remission in global airway disease. Gangemi and Manti et al. present an operational landscape that integrates cellular remodeling pathways, structural readouts, and digital biomarkers with advanced AI to drive disease modification in severe asthma. Matsuyama et al. show that IL-33, together with oxidised low-density lipoprotein and complement fragments, drives inflammatory extracellular trap formation in eosinophils. Kumar and Chan et al. link small airways dysfunction to reduced rates of asthma remission. Wen et al. demonstrate that seven genes and two Weighted Gene Co-Expression Network Analysis (WGCNA) modules are consistently elevated in asthma across both the lower and upper airways. Andersson et al. find significant associations in BMI, sex and steroid treatment on circulating adipokine levels, highlighting the complexity of mechanisms underlying obesity-related asthma and adipose-related adipokine dysregulation. Pathinayake et al. show that resolving endoplasmic reticulum protein misfolding restores corticosteroid sensitivity in experimental models of severe, steroid-resistant asthma. Cannata et al. reveal that MAIT cells suppress IgE-mediated asthma through an IFNγ-dependent regulation of B cells. Pyung and Kang et al. identify three metabolite-defined subgroups of clinically stable asthma with distinct lung function, airway structure, and immune profiles. Wechsler et al. report that dupilumab reduces circulating type 2 biomarkers and improves lung function in persistent asthma. Song and Kermani et al. examine the role of cellular senescence in severe asthma. Yang and Seo et al. find that longer asthma duration is associated with elevated non-type 2 sputum biomarkers and reduced type 2 inflammation in severe asthma. Shen et al. define distinct airway transcriptomic endotypes in type 2 biomarker-high and -low severe asthma, independent of corticosteroid effects. Chae and An et al. identify four plasma metabolomic subgroups of adult asthma with distinct clinical and lipid-metabolism profiles. Declercq et al. establish chitin as a potent adjuvant for type 2 airway inflammation, independent of endogenous chitinolytic activity. ...continued in the comments journalallergy.com