We therefore examined the novel process of MCET formation and regulation by PAD4, and their contribution to inflammation, vascular function, and acute and chronic pain in SCD using the well-established humanized HbSS-Berkeley (BERK) “sickle” mouse model that shows the characteristic features of sickle cell pathobiology and pain (hyperalgesia). Here, PADI4 is linked to Schnyder corneal dystrophy.