In parallel, Lipchick et al. reported that MM cells can reprogram their metabolism to develop PI resistance by inhibiting lipid synthesis, as demonstrated by the findings that levels of SREBP1, along with its downstream target fatty acid elongase 6 (ELOVL6), were lower in bortezomib-resistant than sensitive primary MM cells, reducing lipid synthesis and causing bortezomib resistance [80]. The gene discussed is SREBF1; the disease is Miyoshi myopathy.