In addition, cells isolated from cirrhotic livers exhibited a phenotype that matched their pathologic situation (hepatocytes: reduced albumin synthesis,42 LSEC: lack of fenestrae,43 HMΦ: inflammatory hyperesponse,44 HSC: increased α‐SMA expression45) suggesting that, unlike other protocols where selection is based on surface markers that may change during cirrhosis (CD31, CD32b)33 our protocol is phenotype‐unbiased and thus suitable for the study of different models of CLD. This evidence concerns the gene ACTA1 and congenital secretory chloride diarrhea 1.