PRNP and prion disease: The remaining 10–15% of human prion disease cases are mainly due to genetic forms, linked to point or insertional mutations in the prion protein gene PRNP. Although of high concern to public health, acquired forms, due to inadvertent human-to-human transmission or zoonotic transmission, are the rarest [4,5].The clinical presentation and disease course of sCJD, broadly correlate with six molecular subtypes usually referred to as sCJD MM1/MV1, MM2c (c for cortical), MM2t (t for thalamic), MV2, VV1, and VV2.