Gastrointestinal mucositis closely follows the paradigm of an acute mucosal damage phase characterized by inflammation, generation of reactive oxygen species (ROS), producing proteins, such as tumor necrosis factor (TNF), interleukin-1β (IL-1β) and interleukin-6 (IL-6), epithelial cell apoptosis, and ulcerative lesions, followed by a self-healing phase with restoration of mucosal epithelium and barrier function [12], [13]. Here, TNF is linked to gastrointestinal mucositis.