EGFR and neoplasm: One additional commonality in our studies exploring the molecular mechanisms by which (ruxolitinib + ERBB inhibitors) killed tumor cells, based on our siRNA analyses of ERBB family receptors, was the importance of signaling through ERBB3, a receptor lacking tyrosine kinase activity but containing six sites of tyrosine phosphorylation that can become acceptor sites for the p85 SH2 domain of PI3K (36, 37).