To date, over 90 genetic mutations in LCAT have been described and are responsible for two phenotypes of LCAT deficiency: fish-eye disease (FED), wherein patients retain residual LCAT activity, particularly on apoB-containing lipoproteins, and familial LCAT deficiency (FLD), wherein patients exhibit a total loss of LCAT activity (Kuivenhoven et al., 1997; Rousset et al., 2009). This evidence concerns the gene APOB and LCAT deficiency.