However, post-mortem examinations showed that neuropathological and biochemical findings did not neatly conform to any of the principal subtypes (MM/MV1, VV2, MV2K with kuru type amyloid plaques; MM/MV2C with predominant cortical pathology with confluent vacuoles and perivacuolar PrP staining; MM2T with prominent thalamic pathology and atrophy; and VV1) [2,6,12]. The gene discussed is PRNP; the disease is amyloidosis.