Mutations  in  the  ras  proto-oncogene  that  substitute arginine for
   either GTPase at amino acid 12 or for glycine at amino acid 61 convert
   the gene into an oncogene (K-ras and N-ras) by inactivating its GTPase
   function,  thus  keeping  the  protein in a perpetual active state and
   promoting abnormal cell division.