Furthermore, co-expression analyses showed that VECs from the fibrosa highly co-expressed FOSB, EGR1, and other AP-1-complex-related transcription factors such as FOS, JUN, JUNB, and ATF3 (Figure 6F), whereas VECs from the ventricularis did not, suggesting their regulatory potential in the side-dependent pathophysiology of CAVD. The gene discussed is JUNB; the disease is congenital bilateral aplasia of vas deferens from CFTR mutation.