Since then, his team made several important contributions in understanding the molecular regulation of cellular hierarchy and plasticity of GSCs as well as therapeutic targeting of GSCs resulting in high-profile papers in Cell, Cancer Cell, Cell Stem Cell, Nature Cell Biology, JEM, Science Translational Medicine, Nature Cancer, and Nature Communications. His lab discovered that: (1) BMX-mediated STAT3 activation is required for maintaining the self-renewal and tumorigenic potential of GSCs (Cancer Cell, 2011); (2) GSCs generate the majority of vascular pericytes to support tumor vasculature and malignant growth in GBM (Cell, 2013); (3) Targeting GSC-derived pericytes disrupts the blood-tumor barrier (BTB) and enhances drug delivery into GBM to improve chemotherapeutic efficacy (Cell Stem Cell, 2017); (4) GSCs and tumor-associated macrophages (TAMs) interplay through several bi-directional signaling to support malignant growth in GBM (Nat. Cell Biol., 2015; Nat. Commun., 2017; 2020); (5) Targeting GSCs through BMX inhibition by Ibrutinib potently suppresses tumor growth and synergizes with radiation to improve therapeutic efficacy for GBM (Sci. Trans. Med. 10:eahh6818, 2018), which led to an ongoing clinical trial using Ibrutinib plus radiation for GBM treatment (NCT03535350); and (6) BACE1 inhibition reprograms tumor-associated macrophages (TAM) and potently inhibits GBM tumor growth (Nature Cancer, 2021). The goal of his research is to develop novel therapeutics targeting GSCs, the BTB, and tumor-promoting TAMs (pTAMs) to effectively improve GBM treatment and the patient survival.