Regardless of the mutation type, in the majority of NF1-affected cases, mutations lead to a loss of neurofibromin GTPase-activating function, resulting in sustainably high GTP-bound levels of RAS proteins and thereby in a continuous tumor-promoting signaling process via RTK-RAS and PI3K/AKT pathway hyperactivation [87,88,89,90]. The gene discussed is AKT1; the disease is neoplasm.