Collectively, our data argue that after (ruxolitinib + afatinib) drug combination exposure, an ERBB1-(ERK + AKT)-NFκB pathway becomes activated in surviving BT474 cells to promote “recurrent” tumor growth; as BAD S112 phosphorylation is increased, this pathway also likely acts to reduce the apoptotic threshold by inactivating BAD. The gene discussed is BAD; the disease is neoplasm.