Chymase contributes to the activation of TGF-b ; thus, the functional polymorphism affecting the expression of the chymase gene may influence the activation of TGF-b and thereby modify the cardiac remodeling response to pressure overload in men. Therefore, in our study, we found an association between the rs1956923 polymorphism in the promoter region of the CMA1 gene and the LV mass and LVDD but not IVST, PWD, and RWT in the group of male patients only. To date, only a few studies have evaluated the impact of genetic polymorphisms on LVH in patients with aortic stenosis, and all of these studies had too-small sample sizes and were thus unable to minimize both false positive and false negative errors, stratify for gender, and test for truth associations. Interestingly, one study showed a minor trend of the G allele of rs1800875 toward a lower LVM/BSA in an additive genetic model in all patients, but the difference did not reach statistical significance. Our study size and design allowed us to address the weaknesses of the former studies. The htSNPs were selected to maximally account for the genetic variation in the CMA1 gene and to perform single SNP and complementary haplotype analysis to decrease the false negative errors. During Pavlovian fear conditioning an initially innocuous stimulus is repeatedly paired with an aversive outcome. This relatively simple learning event engages multiple psychological and physiological response systems. For example, individuals quickly acquire the ability to explicitly state the nature of the cueoutcome relationship during training. At the same time they develop a conditioned emotional response that can be expressed later when they again encounter the danger signal. When the CS and the UCS are separated by a temporal gap, as in the “trace” conditioning procedure, people can only develop conditioned responses if they are also able to explicitly state, and are thus consciously aware of, the contingent relationship between stimuli. Based on these results it is assumed that because subjects are not directly experiencing the CS during the presentation of the UCS, they must be able to accurately maintain the CS in memory until the presentation of the UCS in order to bridge the temporal gap between these two stimuli. In this paper we challenge the generality of this assumption by training subjects to fear unperceived faces. There is a broad literature suggesting that the amygdala shows a specific sensitivity to faces and other “prepared” stimuli, that these stimuli are better at predicting aversive outcomes than other signals, and that training with these stimuli lead to a fear memory that is more difficult to extinguish. Although fearful or angry stimuli are often thought of as “prepared stimuli”, recent work from our lab suggests that even neutral faces strongly activate the amygdala.