As we have noted recently the tumor micro-environment, including local immune cells, can protect tumors, especially from checkpoint inhibitors. As CancerNetwork has noted:
The trial was an international, multicenter study that enrolled 65 
patients with metastatic pancreatic ductal adenocarcinoma who were 
previously treated with either fluorouracil-based or gemcitabine-based 
treatment in the first-line setting. Patients were randomly assigned to 
receive either single-agent durvalumab, an anti–programmed death-ligand 1
 (anti–PD-L1), or durvalumab in combination with tremelimumab, an 
anticytotoxic T-lymphocyte–associated antigen 4 (CTLA-4)....Although immune checkpoint inhibitor combination therapy has shown 
efficacy for immunogenic, “hot” tumors, such as melanoma and lung 
cancer, one key difference is that pancreatic cancer is not an 
immunogenic tumor, commonly known as a “cold” tumor. “There are not a lot of immune cells within the pancreatic cancer,” ..., nothing that there are also immunosuppressive signals. “The 
question is how do we facilitate bringing in these immune cells?” ... combining immune checkpoint inhibitors may not be the 
answer. Instead, it may require a “multipronged approached,” one that 
involves different types of agents, such as vaccines or oncolytic 
viruses, that can prime the immune microenvironment so that the 
checkpoint inhibitors can then work.
This is interesting. It may be that certain cold tumors are protected by the immune system. Just a thought.
