Moreover, authors (102, 103) have recently suggested that vitamin C may interact with molecular pathways related to inflammatory stress and immune dysfunction during sepsis, involving particular mediators: Epidermal Growth Factor Receptor (EGFR), Mitogen-Activated Protein Kinase-1 (MAPK1), Proto-Oncogene c (JUN), C–C chemokine Receptor type 5 (CCR5), Mitogen Activated Protein Kinase 3 (MAPK3), Angiotensin II Receptor type 2 (AGTR2), and Signal Transducer and Activator of Transcription-3 (STAT3). This evidence concerns the gene EGFR and Sepsis.