For example, in malignant melanoma the most common oncogenic mutations at Gln-61 in NRAS (Q61R,K) are predicted to disable the guanine exchange factor SOS1 (as previously reported24) and activator RASA1 interactions, whereas in pancreatic carcinoma KRAS mutations are more enabling of both of these proteins (Fig. S6b,c). This evidence concerns the gene RASA1 and exocrine pancreatic carcinoma.