The major sources of reactive oxygen species in acute liver failure include KCs, neutrophils, and dysfunctional mitochondria [8], and, accordingly, KC depletion alleviates acute liver injury induced by ischemia/reperfusion (I/R) [9], concanavalin A (Con-A) [10], or lipopolysaccharide [11]. The gene discussed is TBCE; the disease is acute liver failure.