In contrast, in p53-deficient tumors, CXCL10 may assume a role in promoting cell survival and drug resistance, primarily through the activation of the PI3K/Akt pathway, which supports tumor progression.42,43 CXCL10 also exhibits a reciprocal relationship with NF-κB signaling, as it is not only induced by NF-κB activation but can also enhance and sustain NF-κB activity, creating a feedback loop that amplifies inflammatory signaling within the TME. Here, AKT1 is linked to neoplasm.