Intracellularly, β2-integrin/kindlin-3 signaling restricts the mature, migratory phenotype of dendritic cells, and abolishing the β2-integrin/kindlin-3 interaction leads to increased expression of maturity markers, increased migration speed in 3D towards CCL19, increased IL-12a production and induction of superior anti-tumor responses in B16.OVA and B16.F10 melanoma models in vivo (177, 193). The gene discussed is FERMT3; the disease is neoplasm.