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We show that response inhibition, and differences between AD(H)D subtypes, exhibit distinct patterns of (at least) three factors (i) strength of pre-trial (pro-active control) theta-band activity, (ii) the inter-relation of pro-active control and inhibition-relation theta band activity and (iii) the functional neuroanatomical region active during theta-related pro-active control processes. This multi-factorial pattern is captured by AD(H)D subtype clinical symptom clusters. The study provides a first hint that