Evaluating topological indexes of the extended regulatory network, we found that the protein kinases MAPK1 and GSK3B and the nuclear receptor RXRA (a type of retinoid X receptor) appear to play key roles in AAA pathogenetic mechanisms, and thus may be intended for interference therapy, as they are “non-hub” connecting proteins that could regulate signaling through the “hub” TFs. The gene discussed is WEE1; the disease is triple-A syndrome.