At the same time, while our data are consistent with the previous publications, indicating that deletion of CTSL in the LDLR−/− mice reduces diet-induced atherosclerosis [8], and increased expression of CTSL in the ECs, VSMCs, and macrophages were observed in human atherosclerotic plaques [31], the same data also provide insights into the signal transduction pathway that leads to atherosclerosis-associated cellular senescence. This evidence concerns the gene LDLR and atherosclerosis.