In an early stage, CatG-deficient mice have an impaired wound healing capacity (Abbott et al., 1998) and neutrophil-derived CatG has been documented to promote myeloid cell adhesion to the arterial endothelium and contributes to atherosclerosis development, suggesting a partial blockade of CatG activity in patients with cardiovascular risk or concomitant inflammatory comorbidities (Ortega-Gomez et al., 2016). Here, CTSG is linked to atherosclerosis.