Given that macrophages in the splenic and hepatic TME have the most potent capacity among myeloid subsets to support T-ALL14, the observed reduction of leukemic burden and prolonged survival following FAK/PYK2 inhibitor treatment likely resulted mainly from reduced FAK/PYK2 signaling in T-ALL cells, rather than altered myeloid composition; however, we cannot rule out that these inhibitors impact other cell types expressing FAK/PYK2, such as leukemia-supportive myeloid cells, thus indirectly reducing T-ALL burden. The gene discussed is PTK2B; the disease is leukemia.