This indicates some redundancy in the roles of the four cancer-associated Ras isoforms (splice isoforms K-Ras4A and K-Ras4B, N-Ras and H-Ras), which is further complicated by the fact that all Ras are capable of engaging the same set of effectors, notably of the MAPK- and PI3K/mTORC1-pathways [51]. Here, HRAS is linked to cancer.