Somatic mutations (A1004S point mutations) and splicing variants of FAK have been reported in 7.7% of human NSCLC (Figure 3B) [112] and they have been shown to exhibit increased autophosphorylation and increased sensitivity to FAK kinase inhibitors as compared with wild-type FAK in patient-derived xenograft models [112]. Here, PTK2 is linked to non-small cell lung carcinoma.