Furthermore, platelets have been shown to be able to influence macrophage polarization toward a pro‐inflammatory phenotype in the context of sepsis.[19] Platelets have also been shown to play a similar pathological role in CKD through modulation of inflammation through secreted factors and interaction with immune cells including macrophages.[20] This is mediated through secretion of both pro‐inflammatory factors such as IL‐1β, CD40 Ligand (CD40L), and CCL5 as well as pro‐fibrotic factors such as TGF‐β and PDGFs. This evidence concerns the gene CD40LG and Sepsis.