Neuropilin-2b facilitates resistance to tyrosine kinase inhibitors in non–small cell lung cancer

Schematic model demonstrating the relationship between EGFR mutant lung tumors and activation of AKT, a kinase linked to cell survival and migration. Pharmacologic inhibition of EGFR blocks activation of AKT. In the presence of NRP2b, AKT remains active via a pathway of NRP2b-dependent activation of GSK3β-mediated degradation of PTEN. Thus, NRP2b potentiates cell survival.