On the contrary, attachment and activation of platelets is associated with platelet-derived GPIbα (Haemmerle et al., 2018), as confirmed by the improvement of steatosis, hepatic injury, triglycerides content, fibrosis and leukocytes infiltration when the major ligand binding domain of GPIbα is blocked, reducing the interaction with Kupffer cells. Here, GP1BA is linked to steatosis.