Additionally, cachectic C26 tumor‐bearing mouse hearts showed decreased PPARα, decreased CPT1β, an alpha‐ to beta‐ myosin heavy chain isoform switch (i.e., adult to fetal), and a switch in glucose transporters from GLUT4 (adult) to GLUT1 (fetal), indicating a decreased reliance on fatty acids and increased reliance on less energetically favorable glycolytic metabolism. The gene discussed is SLC2A1; the disease is neoplasm.