Although point mutations are rare in ovarian tumors, a hallmark of this cancer type is the mutation of the tumor suppressor P53 with over 94% in HGSOC [53], which could correlate with a loss of the tumor suppression function of P53, including cell cycle inhibition, apoptosis, senescence, DNA repair and autophagy, as well as processes that oppose oncogenic metabolic reprogramming [54]. Here, TP53 is linked to neoplasm.