CD69 and lymphoma: While previous studies have reported context-dependent immunostimulatory effects of mTOR inhibition,74 these findings have typically been limited to phenotypic assays or focused on a few inflammatory markers.75–81 Similar to our observation, rapamycin-treated activated human B cells displayed an activated phenotype with increased numbers of CD23-, CD25-, and CD69-expressing cells.81 Our study expands this by providing a genome-wide transcriptomic perspective in both lymphoma and primary B cells, revealing the extent and scale of immune gene upregulation upon mTOR inhibition.