ABCA1 and asthma: In future strategies aimed at metabolically reprogramming macrophages in asthma, a key challenge will be to precisely modulate this coupled glucose–lipid metabolic axis according to disease etiology and stage—for example, downregulating M1-associated SLC25A1/ACLY activity during acute exacerbations or infection-related phenotypes, while optimizing ABCA1-mediated lipid efflux and M2 oxidative metabolism during chronic remodeling—to enable truly phenotype-guided therapy (Albers et al., 2025; Infantino et al., 2014).