Objectives Because post-transcriptional mechanisms modulate levels of p16 (encoded by CDKN2A ) and p15 (encoded by CDKN2B ), we tested whether interferon- (cid:1) regulates the expression of these proteins and the effect of the 9p21 genotype. Background The mechanism whereby the common variant at chromosome 9p21.3 confers risk for coronary artery disease (CAD) remains uncertain. A recent report proposed that 9p21.3 confers differential activation of adjacent genes in response to interferon- (cid:1) , and reported that mRNA levels of CDKN2B are reduced in response to interferon- (cid:1) . Human umbilical vein endothelial cells (HUVECs), aortic smooth muscle cells, HeLa cells, HEK293 cells, and 16 human lymphoblastoid cell lines, all genotyped for the 9p21.3 locus, were treated with interferon- (cid:1) and ana-lyzed by immunoblot. Results In all cells tested—except HUVECs where expression was not modulated by interferon- (cid:1) —regardless of 9p21.3 genotype, interferon- (cid:1) increased the expression of p16 and p15. Northern blot analysis confirmed that interferon- (cid:1) has little effect on mRNA levels of CDKN2A and CDKN2B . 9p21.3 p16 interferon-