STAT3 and glioblastoma: Notably, these signaling mechanisms may reciprocally influence one another: for instance, it has been shown that NF-kB may induce the expression of the suppressor of cytokine signaling (SOCS)3, in turn inactivating STAT3 in human glioblastoma cells [80], and that NFAT may engage with STAT3 in a dynamic ternary complex promoting the hypertrophy of cardiomyocytes in mouse models [81].