That somatic mutations in the PLXNA1 receptor might exert similar downstream effects usually as seen after ligand stimulation is also supported by the observation of increased phospho-Erk levels and unchanged E-cadherin and MMP-9 levels between SEMA3A-stimulated and untreated pancreas cancer cells including Panc1 described in a prior report [12]. This evidence concerns the gene SEMA3A and pancreatic neoplasm.