We found via multiplex assays that the pro-apoptotic protein BAD was hyper-phosphorylated in tumors previously exposed to (ruxolitinib + afatinib), and is phosphorylated on Serine 112 by ERK1/2; in preliminary studies the drug combination reduced BAD S112 phosphorylation in these tumor cells by ~50%; knock down of BAD reduced the lethality of (ruxolitinib + afatinib) and also reduced drug-induced activation of BAX [Observations1]. The gene discussed is BAX; the disease is neoplasm.