In marked contrast to oncogenic KRAS-induced pancreatic cancers, which are influenced heavily by obesity but not leptin14, or to pathogen infections that can elicit transient changes in local adipose tissue/leptin levels that affect wound repair46, malignant progression in HRAS-induced cutaneous cancers requires the induction of LEPR signalling by the stem cells, but neither obesity nor adipogenesis in the local tissue environment. This evidence concerns the gene KRAS and pancreatic neoplasm.