However, this interaction was evident only in the presence of both the “Swedish” mutation in APP, which increases production of the 99-amino acid C-terminus of APP that is a direct substrate for γ-secretase and of apoE, indicating a differential cellular interaction of TMCC2 not only with AD-risk versus normal forms of apoE, but also of APP [16]. The gene discussed is TMCC2; the disease is Alzheimer disease.