It must be pointed out that GEP analysis performed on PTX3-expressing MM cells indicates that (i) the increased PTX3/FGF2 ratio appears to be due to PTX3 overexpression and not to PTX3-mediated FGF2 downregulation and (ii) the antiangiogenic response is due to the FGF-trap activity exerted by PTX3 rather than to a modulation of the expression of other pro- or anti-angiogenic factors caused by PTX3 overexpression. The gene discussed is FGF2; the disease is Miyoshi myopathy.