The results indicated that, besides exerting in vitro antiproliferative and apoptotic effects, EA possesses additive or synergistic growth inhibitory activity in combination with mitomycin C. Treatment with EA also inhibits tumor cell invasion of the extracellular matrix components in response to VEGF-A, likely through down-regulation of VEGF receptor type 2 (VEGFR-2) levels, and modulates the expression of the immune checkpoint protein PD-L1. This evidence concerns the gene CD274 and neoplasm.