Loss of Acat1 in NSCLC cells impedes TLS and anti-tumor immunotherapy ACAT1 increases intratumoral oxidative stress by promoting mitochondrial hypersuccinylation Reduction of oxidative stress promotes B cell aggregation to build the TLS ACAT1 correlates with TLS abundance and immunotherapeutic response of NSCLC patients. Here, ACAT1 is linked to neoplasm.