By current criteria, bronchioloalveolar carcinoma (BAC) is a subtype of pulmonary adenocarcinoma, developing from terminal bronchiolar and acinar epithelia and progressing in a lepidic and/or aerogenous manner on intact alveolar walls but without stromal, vascular, or pleural invasion. Evidence suggests that the 2 main cytologic types of BAC, ie, nonmucinous and mucinous, have some differing characteristics. The more frequent nonmucinous BAC directly evolves from the terminal respiratory unit cells, the type II pneumocyte, and Clara cells. This form predominates in smokers, presents more frequently as a ground-glass opacity, and frequently harbors epidermal growth factor receptor (EGFR) polysomy/mutations, believed to be the driver of its malignant process. The less frequent mucinous BAC, on the other hand, derived from metaplasia of bronchiolar epithelia, presents more frequently as a pneumonic-type infiltrate, rarely demonstrates EGFR polysomy/mutations, and much more frequently harbors and is driven by a K-ras mutation. These mutational oncogenic differences could lead to different therapeutic responses: nonmucinous BAC has been found to be sensitive to EGFR tyrosine kinase inhibitors, while mucinous BAC might be more responsive to taxane-based chemotherapy. In fact, there might be more differences than similarities, suggesting 2 distinct phenotypes that might need to be treated differently in order to optimize our management of the range of clinical disease that is often currently broadly classified as BAC.