The ensuing compromising of tight junction integrity and IL‐1β‐ and MyD88‐dependent increased vascular permeability has been proposed to promote CM pathogenesis.119 In support of this, HRP‐2 has been shown to line the endothelial walls of blood vessels,120 particularly in retinopathy‐positive CM patients.121 Once the BBB is disrupted, leukocytes, cytokines, chemokines, and soluble parasite products may enter the brain parenchyma to activate the microglia and damage astrocytes and neurons, causing neuro‐inflammation and coma.122. Here, HDGFL2 is linked to cutaneous mastocytosis.