In addition to chronic/continuous exposure to IFNs, as aforementioned, constitutive activation of the JAK-STAT pathway could also occur as a result of stimulation of other extracellular signals (e.g., IL-6 and IL-10) [76], cell-intrinsic changes associated with non-receptor tyrosine kinases (NRTKs) such as Src and cytoplasmic kinases (protein kinase C) [77], as well as special cellular components in the TME (e.g., astrocytes in GBM) [78], contributing to radioresistance. The gene discussed is SOAT1; the disease is glioblastoma.