First, we probed the impact of PDCD1 deletions on (PI3K)–AKT–mTOR signaling and glucose uptake based on six individual patients, three with mutant PDCD1 and three with wild-type PDCD1. In line with our findings in the murine model, PDCD1-mutant lymphoma cells exhibited a significant increase in S6 ribosomal protein phosphorylation, demonstrating enhanced mTOR activity compared to PDCD1-wild-type cells (Fig. 7c; P = 0.0309)54. This evidence concerns the gene AKT1 and lymphoma.