In vivo studies have demonstrated that Gal-3 expression in the lungs is up-regulated during allergic asthma and Gal-3 deficient (Gal-3-/-) mice exhibit significantly reduced pulmonary eosinophilia and airway hyperresponsiveness (AHR) in response to acute allergen [ovalbumin (OVA)] challenge relative to wild-type (WT) mice (Zuberi et al., 2004). This evidence concerns the gene LGALS3 and allergic asthma.