Among PLAs, the accumulation of the PLA2G16 isoform was observed in the lung nodules and in the renal angiomyolipomas of LAM patients, and it was demonstrated that the presence of tuberin negatively regulates PLA2G16 overexpression both in vitro and in vivo, affecting also the production of prostaglandins, that are critical mediators of chronic inflammation and cancer progression. Here, PLAAT3 is linked to kidney angiomyolipoma.