Phosphorylation favors accumulation on the GTP-loaded state because of Improved intrinsic nucleotide-exchange level and impaired GTP hydrolysis. We suggest below that resistance to SHP2 inhibitors of KRAS Q61H cells stems from these special functions, which manage MAPK signaling even when KRAS is phosphorylated, together with SOS GEF and RASA1 GAP https://barryz086blu6.digitollblog.com/profile