Sepsis is a severe, life-threatening disease that affects multiple organ systems and causes numerous damages throughout the organism. However, the mechanisms of sepsis and the body's defenses are not fully understood. Many studies describe the involvement of the immune system in the development of sepsis, but the involvement of platelets in the development and defense of sepsis is elusive. Moreover, thrombocytopenia is frequent in septic patients and is a marker of poor prognosis and a high risk of death in sepsis. Therefore, in this work, by analyzing the transcriptome of patients suffering from sepsis based on available data, we investigated differences in the levels of selected transcripts potentially important for platelet function and sepsis. We analyzed thrombospondin 1 (TSP1), a major protein component of platelet α-granules, and ADAR (adenosine deaminase acting on RNA, 1-3), a group of proteins not previously studied in platelets. We found that transcript levels for TSP1 or ADAR2 and 3 did not change, whereas they increased significantly only for ADAR1 in platelets from septic patients. Next, we performed in vitro analysis of platelet precursor cells and mouse megakaryocytes for TSP1 and ADAR1. We found that TSP1 expression increases as megakaryocytes differentiate into platelets. Culturing megakaryocytes with interleukin 1α (IL1α, cytokine involved in sepsis) did not change TSP1 levels. Unfortunately, we could not detect ADAR1 in mouse megakaryocytes with available antibodies. Future studies are needed to explain the role of these proteins in platelets and their involvement in sepsis.