COL3A1 and Ehlers-Danlos syndrome, vascular type: Using two heterozygous Col3a1 mutations-carrying mouse models of vEDS (Col3a1G209S/+ and Col3a1G938D/+), Bowen et al. [26] demonstrated that abnormalities in this signaling pathway are likely involved in spontaneous vascular events in the setting of vEDS, as pharmacologic inhibition of PKCβ or ERK1/2 led to better outcomes in mutated mice by preventing spontaneous fatal aortic rupture.