Moreover, although we have found that CMH increases histone acetylations up to 16 h of exposure of IPF fibroblasts (Supplementary Figure S1), as is the case in cancer cell by HDAC3, 6 and 8 inhibition [41], it may downregulate FLIP by inhibition of SIRT1-mediated deacetylation of nonhistone proteins as Ku70 [23], which is a key function of SIRT1 [24]. This evidence concerns the gene HDAC3 and idiopathic pulmonary fibrosis.