Additionally, other parallel mechanisms, such as the loss of heterozygosity of the p53 gene with a concomitant deletion of 17p13.1 that is known to drive aggressive tumor phenotypes, could potentially promote arachidonic acid accumulation as a result of an incidental deletion of ALOX12/15 genes51 and provide another therapeutic opportunity for niclosamide in the treatment of this subset of aggressive human tumors. Here, ALOX12 is linked to neoplasm.