However, in response to increased cardiac stress, the expression of the ATE1 gene and protein in adult rats was strongly upregulated, and the loss of ATE1 gene expression in this type of cardiac cells suppressed the expression of genes that regulate cardiac hypertrophy [9]; this effect may be potentially related to downregulation of arginylation after ATE1 knockout or silencing, which makes the cells less sensitive to different stress factors [39]. The gene discussed is ATE1; the disease is cardiac hypertrophy.