In contrast, patients with the mirror‐image phenotype, namely recessive abetalipoproteinemia or homozygous hypobetalipoproteinemia, due to pathogenic variants in the MTTP or APOB gene, respectively, characterised by failure to produce and secrete apo B‐containing lipoproteins, are protected from ASCVD but can sometimes display hepatic steatosis and eventually hepatic fibrosis [6, 7, 8]. This evidence concerns the gene APOB and abetalipoproteinemia.