While we acknowledge the contribution of microglia and other leukocytes to SPI1/PU.1 upregulation in TSC tubers, we conclude that SPI1/PU.1 in malformed cells with intrinsic mTOR activation drives the execution of immunogenic transcriptional programs normally only present in microglia, promoting the expression of pro‐inflammatory factors such as complement or cytokines. The gene discussed is SPI1; the disease is tuberous sclerosis.