LEP and pancreatic neoplasm: 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.