In this GBM model, PTEN deficiency regulates lysyl oxidase expression, which functions as a macrophage chemoattractant via activation of the integrin β1‐PYK2 axis.[69] Hence, development of a highly potent, selective inhibitor for PYK2 could have a therapeutic impact, especially since PYK2 and its most related kinase FAK have overlapping, but still distinct functions,[70, 71] particularly in immune cells including macrophages. The gene discussed is PTK2; the disease is glioblastoma.