Of note, in previous studies in murine models of toxic-induced liver fibrosis, we observed that CTSB inhibition mitigated chronic CCl4-induced inflammation, hepatic stellate cell (HSC) activation, and collagen deposition.9 Similarly, other studies using both pharmacological and genetic CTSB inactivation observed reduced hepatic inflammation, as assessed by transcripts for CXC-chemokines and neutrophil infiltration after cholestasis.19 However, in both studies, the mechanism behind the pro-inflammatory role of CTSB was lacking. The gene discussed is CTSB; the disease is cholestasis.