MARK2 and cancer: However, in cancer, MAPK signaling is commonly hyperactivated due to gain of function mutations in proto-oncogenes including B-Raf proto-oncogene, serine/threonine kinase (B-Raf) [9], neuroblastoma RAS viral (v-ras) oncogene homolog (NRAS) [10], Kirsten rat sarcoma viral oncogene homolog (KRAS) [11], Raf-1 proto-oncogene, serine/threonine kinase (RAF1) [12], or loss of function mutations to negative regulators including neurofibromatosis type 1 (NF1), in each case leading to enhanced cell proliferation and survival [13].