For instance, it was shown that the KRAS/MAPK/ERK/GLI1 activation could be mediated by either oncogenic KRAS mutation or stimulation of neuropilin 2 (NRP2) by vascular endothelial growth factor (VEGF) in lung adenocarcinoma (LAC) of non-small cell lung cancer (NSCLC). This evidence concerns the gene NRP2 and lung adenocarcinoma.