A dual function of ACSL4 enzyme has been demonstrated in MM, with a tumor promoting function observed when highly expressed in malignant PCs, where its knock-down antagonizes cell proliferation, likely by inhibiting c-Myc and SREBPs transcription factor activity; on the other hand, high expression of ACSL4 is also mandatory for the activation of the ferroptosis pathway: as a consequence, ACSL4 knockdown induced ferroptosis resistance in MM cells, implicating ACSL4 as a predictive biomarker of ferroptosis sensitivity in MM [82]. This evidence concerns the gene ACSL4 and neoplasm.