Deletion of HPK-1 in mice has effects beyond antigen receptor signaling pathways; HPK1-/- bone marrow-derived DCs (BMDC) expressed higher levels of co-stimulatory molecules and pro-inflammatory cytokines and enhanced antigen presentation capacity [15–17], which is consistent with ex vivo evidence for anti-tumor activity in HPK1 null T cells and DCs. Here, MAP4K1 is linked to neoplasm.