RB1 and Guillain-Barre syndrome: The majority of GBs also have genetic abnormalities disrupting the Rb1 pathway, that is, by one of the following: loss of wild-type CDKN2A (generally together with loss of wild-type CDKN2B by homozygous deletion) or loss of wild-type RB1 or amplification and overexpression of CDK4. In addition, losses of wild-type PTEN occur in almost one-half of GB and amplification of EGFR in approximately one-third (Ueki et al, 1996; Rasheed et al, 1997; Schmidt et al, 1999; Ichimura et al, 2000).