Many actinopathies share defects in leukocyte motility (e.g., T cell egress from the thymus, homing of lymphocytes to secondary lymphoid organs, migration towards chemokines, assembly of the uropod of migrating lymphocytes) while others display unique defects specific to certain molecules (e.g., cytothripsis in DOCK8-deficient T cells during interstitial migration). This evidence concerns the gene DOCK8 and alpha-actinopathy.