This relative lack of activity may be a result of two considerations, (1) the preclinical results with JAK-STAT inhibition in GBM are variable, and (2) STAT3 signaling is nuanced since STAT3 can act, paradoxically, as a tumor promoter or suppressor, depending on factors that require further clarification [17, 18]. This evidence concerns the gene SOAT1 and glioblastoma.