In a final fifth set, we noticed mitochondrial stress (LDHA, PKM, COX17, VDAC1, COX8A), an IL2 withdrawal-associated stressed phenotype (MT1E, MT1X), proteotoxic stress (PSMB3/B6/D4/A7/C3, HSPB11, PARK7, EIF4EBP1) and glycolysis (PGAM1) suggesting ‘exhaustion’ at the end of the TH1-like-trajectory.27,28 Overall, in mild COVID-19, the TH1-like-lineage was characterized by increased expression of set 2 genes, indicating increased TH1-effector function. This evidence concerns the gene PKM and COVID-19.