Furthermore, functional analysis suggests that altered DNA methylation of extracellular (e.g., O-glycan processing) and intracellular components contribute to activation of oncogenes (e.g. KRAS and SCL2A1) and suppression of tumor suppressors (e.g. ARHGEF4, EPHB2 and SOCS3), leading to increased oncogenic potency. This evidence concerns the gene KRAS and neoplasm.