Duringtype 2 inflammation, such as in allergic asthma, IL13 signals through STAT (Signal Transducer and Activator of Transcription) proteins to drive pathophysiological changes in the airway epithelium, including increased mucus production, goblet cell metaplasia, and loss of ciliated cells. How these changes are coordinated is poorly understood. Long non-coding RNAs (lncRNAs) do not encode proteins; rather, some produce functional RNA transcripts that are powerful regulators of cellular identity and function. We have developed an approach to test the function of lncRNAs in an air liquid-interface organoid culture system of primary human bronchial epithelial cells (BECs) that recapitulates much of the in vivo physiology of the airway epithelium and its response to type 2 inflammation. Using CRISPR/Cas9, ATAC-Seq and single-cell RNA-Seq, we have identified a lncRNA that coordinates the response of the airway epithelium to IL13 and hypothesize it provides a mechanistic link between IL13 signaling and lung pathology seen in asthma. The work highlights a new role for lncRNAs as central regulators of airway epithelial cell biology, and as potential therapeutic targets for asthma.