SOAT1 and neoplasm: In resistant tumors, CXCL10 may facilitate the recruitment of Treg or MDSCs that dampen antitumor immunity and limit treatment success.46 Therefore, the CXCL10–CXCR3 axis acts as a dynamic modulator of the TME through its integration of JAK/STAT, MAPK/ERK, and PI3K/Akt signaling pathways, with STAT1 playing a central but context-dependent role that can mediate both protective and detrimental outcomes depending on tumor genotype, immune context, and cytokine milieu.