Tumor cells with high levels of PDL1 expression were more sensitive to autophagy inhibitors than cells with lower PDL1 [153]; in gastric cancer, autophagy regulates PDL1 expression through the p62/SQSTM1-NF-κB pathway, while pharmacological inhibition of autophagy increased the levels of PDL1 in gastric cancer cells and in xenografts models, influencing the therapeutic efficacy of PDL1 inhibitors [154]. This evidence concerns the gene SQSTM1 and neoplasm.