This implicates RAS/MAPK signaling in the NB tumour-suppressing effects of NGF-activated TrkA receptors and PI3K/Akt/NF-κB without RAS/MAPK signaling in the diametrically opposed oncogenic activity of TrkAIII, which for some reason is unable to activate the RAS/MAPK pathway, despite binding Grb-2 and Frs-2 adapter proteins involved in RAS/MAPK activation [43]. The gene discussed is AKT1; the disease is neoplasm.