These include but are not limited to activation of the JAK/STAT signaling pathway resulting in PD-L1 upregulation [26], the recruitment of granulocytic myeloid-derived suppressor cells (MDSCs) to the tumor microenvironment following ICI therapy through the IFN-γ-dependent activation of the inflammasome pathway [27], and immunosuppressive enzyme indoleamine 2,3-dioxygenase (IDO1) induction and depletion of effector T cells by activation-induced cell death [28]. This evidence concerns the gene SOAT1 and neoplasm.