Combining the two studies confirmed that S variants associated with reductions in apoA-I (P = 0.03), and showed that variants suspected of (A164S) or previously associated with amyloidosis (S36A, F71Y, K107del) tended to have higher levels of apoA-I and HDL cholesterol than variants associated with reduced LCAT activation (L144R) (Figure S2; P-values <0.01). This evidence concerns the gene LCAT and amyloidosis.