Interestingly, previous work demonstrated that atherosclerosis is reduced in a double knockout model of Egr-1 and ApoE mice, as compared with that observed in the ApoE−/− knockout model only, thus suggesting that lack of Egr-1 is protective in the absence of ApoE.32 Our study extends this evidence by demonstrating that Egr-1 can be upstream of ApoE, negatively regulating its expression. Here, EGR1 is linked to atherosclerosis.