This shared upregulation of IFN-induced STAT1 signaling led to divergent expression of downstream effector proteins such as IL-6 and M×1 (Figure 5A), both of which are known to mediate tumor cell resistance to immune effector cell-mediated attack.42,43 We examined whether inhibition of STAT1 signaling could enhance ADCC sensitivity and possibly reverse ADCC resistance. This evidence concerns the gene STAT1 and neoplasm.