Phosphorylation at Y32 and Y64 by SRC reduces binding capacity of RAS proteins to downstream effectors and in particular decrease the oncogenicity of KRASG12 mutants.160–162 The inhibitory effects by tyrosine phosphorylation can be reversed by SHP2 phosphatase, thus SHP2 has been developed as an important regulatory target for KRAS-driven cancers. This evidence concerns the gene KRAS and cancer.