It can be recognised.
So why does it survive?
More mutations means more for the immune system to see. That is why TMB became a biomarker for immunotherapy.
Yet the tumours in this paper have plenty of mutations, intact antigen presentation โ and no T cells. They can be recognised, and nobody comes.
These twenty lessons are the catalogue of how: not being seen, not being caught, not letting anyone in. And not just the catalogue โ you score each one across 407 TCGA lung adenocarcinomas, check which of the paper's five claims survive in three cohorts, and watch the 'recognition circuit is low' conclusion collapse completely when you account for infiltration.
How you'll learn
There are dozens of evasion mechanisms. We group them by what they cut: not being seen, not being caught, not letting anyone in. Those three are the syllabus for lessons 4 to 15.
The paper links immune-desert tumours to WNT, MYC, EMT, stemness and NF-ฮบB. Score them one by one and only MYC survives โ while EMT comes out in the opposite direction.
'The recognition circuit is low in immune-desert tumours' โ a clean result (โ0.61 vs +0.57). Regress out infiltration and p = 0.94. The difference vanishes entirely. Bulk cannot unmix what is mixed.
A result from one cohort may be a property of that cohort. Ask again in GSE81089 (197) and GSE171415 (35): only MYC and proliferation reproduce, and EMT disappears.