Innervated tumors are frequently more aggressive than less innervated ones. The nervous system is an active participant in carcinogenesis and cancer progression but the mechanistic understanding of how tumors obtain their neural elements remains unclear. Schwann cells, the main population of glial cells of the peripheral nerves, drive and support axonal growth towards the target during development and after injury. These cells are often found disperse in the tumor stroma altering tumor microenvironment and fostering cancer progression. Our previous results demonstrate that the neurotrophic properties of Schwann cells can be modulated by thrombin which acts through its main receptor, the protease activated-receptor-1 (PAR1) (Pompili et al., 2017; Pompili et al., 2020). Aim of the present project is to analyse the contribution of the thrombin/PAR1 axis at the crosstalk between Schwann cells and some neurotropic tumors, such as pancreatic adenocarcinomas. It is imperative to fill knowledge gaps related to comorbidities, mechanisms of pathogenesis, and pathways rendering some tumors, such as pancreatic cancer, refractive to therapy in order to improve the medical management of this deadly disease.