βMCA and (T)UDCA also protect against drug-induced cholestasis, possibly by inducing a signaling cascade by activating protein kinase C (PKC) [38], or blocking DCA-induced nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) activity, as reported in colorectal HCT116 cells, which corresponds to the effects of BBR [21, 39–41]. Here, PRRT2 is linked to cholestasis.