Studies have attributed this to a heterogenous tumor microenvironment that minimizes the number of specific cell surface tumor antigens along with a microenvironment that limits CAR trafficking due to chemokine receptor mismatch, expression of immunosuppressive agents like prostaglandin E2 and cyclooxygenase 2, and presents an unfavorable metabolic environment that severely limits CAR efficacy [30]. This evidence concerns the gene PTGS2 and neoplasm.