For instance, Sharma et al. examined palmitoyl-protein thioesterase 1 (PPT1), focused on in vivo models; the findings exhibited enhanced anti–PD–1 therapeutic response in melanoma prompted through three mechanisms: (1) it facilitates a switch from M2 to M1 macrophage polarization, (2) diminishes the presence of myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment, (3) triggers the release of IFN-β from macrophages, which enhances T-cell-mediated cytotoxicity and increases NK cell infiltration within the tumor microenvironment [156]. This evidence concerns the gene PDCD1 and neoplasm.