In this study, we investigated (a) if NLRP3-mediated inflammation is activated in keloids, (b) whether Glut1 expression is elevated in burn tissue from keloid compared with nonkeloid patients, (c) if glycolytic enzymes are upregulated in burn skin in a similar fashion to keloids, and (d) if the PKM2 inhibitor shikonin downregulates inflammatory markers and glycolytic enzymes in burn skin while sparing normal wound healing. This evidence concerns the gene SLC2A1 and keloid.