The underlying explanation could in part be the effects of putative down-regulation of FLG also in this group, but as the expression of LAMB3 did not reach significance in the AD FLG−/− group and neither did CTNNA1 or LAMB3 in the AD FLG+/− group, other explanations are plausible, including that these genes are candidates for the primary pathogenesis in AD in addition to FLG deficiency. The gene discussed is CTNNA1; the disease is Alzheimer disease.