This, coupled with the observation that COX-2, 5-LOX, and 12/15-LOX are overexpressed in STZ-induced diabetic animals [51] and HETE is increased in diabetes mellitus [53] with a concomitant decrease in LXA4 in the vitreous fluid in DR, suggests that LXA4 can suppress RUNX1–12-HETE expression and action [88,89,90,91,92,93,94,95,96,97]. Here, PTGS2 is linked to diabetes mellitus.