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(Reprinted withpermission from Rubin R, Strayer DS.

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These differences in the clinical signi?cance of Pin1overexpression may be rationalized considering the provocative hypothesis that inbreast cancer the mutant p53 network may be the major determinant of aggressive-ness among the oncogenic mechanisms ampli?ed by Pin1, while in other tumortypes, other mutant p53-independent mechanisms may take over. Opposingly, when tasks involvehigh levels of difficulty, those higher in cognitive reservemay display more neural activation, because they have agreater neural capacity to use when performing the task.Attending to difficulty is thus vital for understandingthe meaning of differences in neural activation betweengroups.

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