Platelets were also associated with the pathogenesis and progression of MA-ARDS, because upon its activation, they release various inflammatory mediators (von Willebrand factor, PF4/CXCL4, RANTES/CCL5) that activate neutrophils, monocytes, macrophages, leukocytes, and endothelial cells, leading to pulmonary endothelial damage (Vieira-de-Abreu et al., 2012; Srivastava, 2014; de Azevedo-Quintanilha et al., 2020). Here, PF4 is linked to microtia.