These include ETS-related gene rearrangements, which interact directly with β-tubulin [34], the induction of p-glycoprotein/ATP-binding cassette subfamily B member 1 to mediate docetaxel efflux [35], decreased docetaxel influx due to SLCO1B3 suppression [36], and the induction of cancer stem cell populations marked by CD44, CD133, and ALDH expression [37]. The gene discussed is LDHA; the disease is cancer.