This appears to have been due to the employment of FAO as an alternative energy source by hepatocytes as well as to an increase in neutral lipid accumulation that has been previously reported in myc−/− fibroblasts, in hematopoietic cells following short-term inhibition of Myc, and in neuroblastomas following treatment with small molecule Myc inhibitors (158, 191, 196). The gene discussed is MYC; the disease is neuroblastoma.