Similarly, Raf1+/L613V and Ptpn11+/D61G mice, as well as K-RasV14I/V14I homozygous mutants, which all model Noonan syndrome, display reduced (or no) survival in the C57BL/6J genetic background, whereas they are viable in a mixed background (Araki et al., 2004; Hernández-Porras et al., 2014, 2015; Wu et al., 2011). This evidence concerns the gene RAF1 and Noonan syndrome.