Peripheral neuropathy is a noxious side effect of many chemotherapeutic agents including taxanes (paclitaxel and docetaxel), but the underlying mechanism of taxane-induced peripheral neuropathy (TIPN) is unknown. Given that taxanes cause cellular apoptosis by binding to β-tubulin and stabilizing microtubules, a process mainly regulated by G protein-coupled receptors (GPCRs), we hypothesize that TIPN is a consequence of taxane binding to β-tubulin and GPCRs and genetic polymorphisms increase TIPN risk by modifying the affinity of this binding. We will examine the hypothesis by virtually screening β-tubulin and GPCRs through a library of >230 neuropathy-inducing chemicals collected by He Lab, using I-TASSER developed by Zhang Lab. Genetic polymorphisms that increase patient’s TIPN risk will be introduced by Dr. Hertz to further validate the drug-protein binding effect. The study expects to provide insights for new therapy developments to reduce neuropathy.