This was found to suppress B-cell–mediated anti-tumor immunity via a metabolic mechanism: loss of Erbin in MKs boosted their mitochondrial oxidative phosphorylation and production of acylcarnitines delivered to B cells, which in turn enhanced B cell metabolic fitness and promoted anti-tumor T-cell responses by facilitating PD-1 degradation on T cells. This evidence concerns the gene ERBIN and neoplasm.