Simultaneous prolonged fever, along with CLABSI, suggests a hypoperfusion mechanism, where sepsis-induced vasoconstriction and hypoxia increase vascular endothelial growth factor (VEGF) expression, leading to increased vascular permeability and ultimately causing vasogenic edema [10,11]. Classical MRI findings of bilateral parieto-occipital hyperintensities on T2-weighted and FLAIR sequences, along with microhemorrhages on SWI, supported the diagnosis of PRES. Here, VEGFA is linked to Posterior Leukoencephalopathy Syndrome.