PROM1 and neoplasm: Our previous studies in the tumor microenvironment (TME) of non-small cell lung cancer revealed that IFN-γ concentration determines pathway activation: high doses trigger classical JAK/STAT signaling, whereas low doses activate ICAM1-PI3K-Akt-Notch1 cascade, increasing CD133 expression and cancer stemness (Song et al., 2019[108]).