Galectin‐3 is a β‐galactoside‐binding animal lectin of appro‐ ximately 30 kDa and is evolutionarily highly conserved. Galectin‐3 is promiscuous, its localization within the tissue micro‐environment may be extracellular, cytoplasmic, or nuclear, and it has a concentration‐dependent ability to be monomeric or form oligomers. These properties impart great flexibility on galectin‐3 as a specific regulator of many biological systems including inflammation. For example, in acute tissue damage galectin‐3 is a key component in the host defense against microbes such as Streptococcus pneumoniae. However, if tissue injury becomes repetitive galectin‐3 also appears to be intimately involved in the transition to chronic inflammation, facilitating the walling off of tissue injury with fibrogenesis and organ scarring. Therefore galectin‐3 can be viewed as a regulatory molecule acting at various stages along the continuum from acute inflammation to chronic inflammation and tissue fibrogenesis. In this review, we examine the role of galectin‐3 in inflammation, and discuss the manipulation of galectin‐3 expression as a potentially novel therapeutic strategy in the treatment of a broad range of inflammatory diseases.