In particular, it is ofclinical relevance, if NTCP or ASBT inhibitors might cross-react withSOAT in a multitarget manner and, therefore, could interfere withthe regulation of steroid-responsive organs.18 Moreover, NTCP/ASBT dual inhibitors might be superior to ASBT-selectiveor NTCP-selective inhibitors for the treatment of cholestatic diseasesbecause apart from protecting hepatocytes from BS overload they alsowould prevent BS accumulation in the renal proximal tubule cells andcholemic nephropathy.32−34 So, in this case, multitarget inhibition might befavorable. The gene discussed is SLC10A1; the disease is Nephropathy.