Consistent with this hypothesis, the immature lungs of our newborn HRAS/NRASDKO animals [19] share similarities, including in particular a significantly increased rate of perinatal lethality, with a murine model of Noonan syndrome harboring a KRASP34R mutation [12], an amino acid which is known to modulate GTP hydrolysis in KRAS proteins (Bera et al. 2020). Here, KRAS is linked to Noonan syndrome.