The activation of the JAK/STAT pathway contributes to IFN-mediated PD-L1 upregulation in several types of cancers.56–58 The activation of the IL-6/JAK1 pathway leads to PD-L1 Y112 phosphorylation and maintains PD-L1 stability.59 Cytokines including IFN-γ, TNF-α, IL-1α, and IL-27 are also able to induce PD-L1 expression in tumor cells.56 58 60 Since the alteration of these pathways might also contribute to the influence of LTX-315 on PD-L1 and it-mediated immune resistance, further studies on the context-dependent action mechanisms of LTX-315 in cancer treatment are still needed. The gene discussed is SOAT1; the disease is cancer.