It is suggested that multiple pathways involving Ras‐related C3 botulinum toxin substrate 1, glycogen synthase kinase 3 beta, and p42/p44 mitogen‐activated protein kinases (MAPK) are responsible for the invasiveness of pancreatic cancer cells upon SEMA3a stimulation.35 However, further investigation shows that this process is independent of E‐cadherin to N‐cadherin switch, MMP‐9, and VEGF induction.35 Interestingly, the influence of NRP‐1 on tumorigenesis is dependent on the genetic status of K‐Ras. The gene discussed is SEMA3A; the disease is pancreatic neoplasm.