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It has beenlong known that there is limited association between the patient’s phenotype and theresidual enzymatic activity, or the amount of lipid stored in the macrophages [ 16 ].When the gene was ? rst identi?ed, there was great excitement that at last the pheno-typic viability associated with this disorder might be explained by the severity of theparticular gene mutation. The chronic phase (Cp) is marked by anincrease in minimally invasive myeloid cells that are mostlyconfined to the hematopoietic tissue, including the peripheralblood, bone marrow, spleen (i.e., splenomegaly), and occa-sionally the liver (i.e., hepatomegaly). Even if a community makes incorrect conclusions,their database may still remain useful for different analyses.
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