Additionally, Suwannakul et al. reported that high expression of GLUT5 in cholangiocarcinoma cells enhanced both fructose utilization and metabolic adaptation, and silencing GLUT5 significantly inhibited tumor cell proliferation, offering a new therapeutic strategy targeting GLUT5-mediated metabolic reprogramming in cholangiocarcinoma 127. The gene discussed is SLC2A5; the disease is neoplasm.