The importance of SLiMs is further corroborated by the occurrence of pathologies that are caused by mutations that either mutate existing linear motifs or create novel linear motifs (of undesired function) (27) . Examples include 'Usher's syndrome' (28) , 'Liddle's Syndrome' (6) or 'Golabi-Ito-Hall Syndrome' (29) . The developmental disorder 'Noonan Syndrome' can be caused by mutations in Raf-1 that abrogate the interaction with 14-3-3 proteins mediated by corresponding SLiMs and thereby deregulate the Raf-1 kinase activity (30) (the Raf-1 protein sequence features two LIG_14-3-3_1 binding sites that are annotated at 256-261 and 618-623 in the ELM resource). A related disease, 'Noonan-like Syndrome', is caused by an S to G mutation at position 2 of the SHOC2 protein, creating a novel myristoylation site (annotated as ELM class MOD_NMyristoyl). This irreversible modification results in aberrant targeting of SHOC2 to the plasma membrane and impaired translocation to the nucleus upon growth factor stimulation (5) . More information about the implication of short linear motifs on diseases is collected at http://elm.eu.org/infos/diseases.html.