PTK2 and neoplasm: Further in vitro and in vivo analyses enabled the creation of a model to explain this increased sensitization to DNA-damaging therapies in cases with FAK-null endothelial cells; specifically, FAK could activate the transcription factor NF-kB in endothelial cells, thus inducing the production of cytokines (i.e., C5, GM-CSF, IL-1α, IL-2, IL-4, IL-6, IL-16, KC, MIG, MIP-2, and TIMP-1), which can support the tumor.