BCR and diffuse large B-cell lymphoma: This includes HGAL’s diverse cellular effects (and their underlying molecular mechanisms) within three key response pathways: (a) HGAL’s differential effects on BCR-activated upstream signaling events (3, 7, 8, 12, 13), enhanced BCR clustering (7, 8), and supramolecular activation cluster (SMAC) formation (8, 10, 14); (b) mechanisms via which HGAL promotes cytoskeletal remodeling, in part through PDZ-RhoGEF recruitment (4, 5, 8, 10, 11, 15, 16); and (c) HGAL as a marker of diffuse large B-cell lymphoma (DLBCL) disease severity (1, 2, 17), and lymphomagenic driver (10, 13, 18).