Decreased plasma LCAT activity is believed to be the likely pathophysiologic mechanism underlying low levels of HDL cholesterol in patients with ALPS as Moraitis and colleagues demonstrated that the HDL subpopulation distribution on native-native 2 gel analysis in a patient with large B cell lymphoma, another lymphoproliferative disorder and disappearing HDL syndrome, was noted to be similar to the profile found in familial LCAT deficiency with predominance of pre-β HDL and α4 HDL particles, absence of larger spherical particles (α1–3), and abnormally low plasma cholesteryl ester [5]. This evidence concerns the gene LCAT and lymphoproliferative syndrome.