The exact etiology of neurologic deficits in patients with PHARC remains unclear, but previous studies have shown that accumulation of lyso-PS in the cerebellum due to disruptive ABHD12 leads to increased levels of microglial activation and neuroinflammation, which is the presumed cause for neurological deficits in abhd12 knockout mice [5,6,7]. This evidence concerns the gene ABHD12 and PHARC syndrome.