SEMA3A and pancreatic neoplasm: Disturbances of the finely-tuned cytoskeletal organization and cytokinesis governed by plexin–semaphorin signaling and other regulators of the axon gene family have previously been shown to foster a malignant evasive phenotype, and it is conceivable that altered plexin receptor A1 function through somatic mutations like D863N tips cell-extending and invading signaling cues by SEMA3A-stimulated plexin signaling towards cell extension, invasion, and growth in pancreatic cancer [40–42].