Recent studies have shown that most cases of Ollier disease are believed to have been caused by isocitrate dhydrogenases IDH1 and IDH2 mutations. In one study, 35 of 43 (81%) patients with Ollier disease had either a IDH1 or IDH2 mutation. Another study suggests that R132C IDH1 mutations which are particularly dominant at exon 4 of IDH genes are linked to the growth of vascular lesions. Isocitrate deyhydrogenases IDH1 and IDH2 are catalysts responsible for the conversion of isocitrate to 2-oxoglutarate. The isocitrate deyhydrogenases IDH1 and IDH2 mutations disrupt this process resulting in unregulated production of α-ketoglutarate and a reduction in chondrocyte proliferation. In many cases of cartilaginous tumors, IDH1 and IDH2 point mutations were found thus explaining why Ollier disease is associated with many different associated conditions. Based on these case studies, most evidence suggests that the abnormal lining of lesions found in Ollier disease would suggest that the condition is caused by a post-zygotic somatic mutation thus resulting in a mosaic genetic disorder.