Thus, we hypothesize that HHcy contributes to AMD via the up-regulation of Glucose transporter-1 (GLUT-1) in RPE cells, inducing a Warburg-like effect in which cells predominantly produce energy by a high rate of glycolysis, rather than by a comparatively low rate of glycolysis followed by oxidation of pyruvate in mitochondria as in most normal cells [31]. The gene discussed is SLC2A1; the disease is age-related macular degeneration.