In this regard, Yang et al. reported that both the computational model docking and experiments showed that DDX5 interacts with UCP2 in H1299 non-small cell lung cancer (NSCLC) cells, and the recruiting of DDX5 with UCP2 at least partially contributes to the metabolic plasticity of NSCLCs via the AKT/mTOR pathway (Fig. 4C) [82]. The gene discussed is MTOR; the disease is non-small cell lung carcinoma.