Objective assessment of adrenocortical carcinoma driver genes and their correlation with tumor pyruvate kinase M2

[Display omitted] •PKM2 may be one of the culprit in ACCs beside its usual nuisances in other cancers.•Inhibition of these six genes may authorize the onset and progression of ACCs.•Understanding the pathophysiological pathway behind ACCs is critical.•Mapping and better understanding of the genetic co-relations are the only way out of these indispositions. Glandular cancers have a significant share of the total cancer patients all over the world. In the case of adrenocortical carcinomas (ACCs), although the benign form is more frequent and common, the malignant form provides a very less percentage of patients with five or more than five years of survival rate. There are gene alterations that are involved as a crucial factor behind the occurrence of ACCs. Out of these, the most prominent genetic alterations (PRKAR-1A, CTNNB1, ZNRF3, TP53, CCNE1 and TERF2 genes) are linked with a glycolytic enzyme pyruvate kinase M2 (PKM2), which converts phosphoenolpyruvate (PEP) to pyruvate in the glycolytic pathway. The involvementof PKM2 renders a cumulative effect through different pathways that may result in the onset of ACCs. Thus, this review aims to establish a link between ACCs, alterations of specific genes and PKM2.