We recently showed that the acyl-coA synthetase long chain 3 (ACSL3), an enzyme that promotes the activation and retention of extracellular unsaturated FAs by converting them into hydrophilic fatty acyl-CoA esters that cannot exit cells [7, 8], is overexpressed in KRAS-driven lung and pancreatic cancer [9, 10]. The gene discussed is KRAS; the disease is pancreatic neoplasm.