Regarding the currently described, specific ability of KRAS to drive RASopathy phenotypes in the absence of the other two (HRAS and NRAS) canonical members of the RAS family, it is pertinent to say that although only KRAS is necessary and sufficient for development to the adult stage [18], our previous transcriptional studies have also documented the critical, specific involvement of HRAS in proliferation, NRAS in immune modulation/host defence and apoptotic responses [48, 49]; and KRAS in cell cycle progression [50, 57]. Here, NRAS is linked to RASopathy.