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Discovery of molecular defects that account for leukocyte adhesion deficiency (LAD) syndromes yield novel insights into mechanisms that govern signaling, targeting, and emigration of leukocyte subtypes, in addition to clinically relevant information relevant to rare but important human diseases. Mutations in FERMT3, leading to deficiency of the protein kindlin-3, account for the disease phenotype in a variant form of LAD (LAD-1v, also called LADIII) in which inside-out signaling of surface integrins is disrupted. For details, see the commentary by Zimmerman on page 4485 and the article by Kuijpers et al on page 4740.