CASP3 and neoplasm: The killing mechanisms induced by the (ruxolitinib + ERBB inhibitor) treatment were many-fold, most notably that (ruxolitinib + ERBB inhibitor) treatment caused a significant greater-than-additive increase in the levels of autophagosome formation that was associated with mitochondrial degradation and activation of caspase 3; as well as autolysosome formation, mitochondrial degradation, AIF translocation to the nucleus, and a necroptotic form of tumor cell death.