Knockdown of GPR109A using siRNA (Supplementary Fig. S7A) demonstrated similar anti-proliferative effects as FAO inhibition, was not further influenced by etomoxir, and was no longer rescued by β-HB (Fig. 4e), validating GPR109A as a primary target of β-HB-mediated cellular proliferation in GBM. The gene discussed is GSTM1; the disease is glioblastoma.