As the reduction in BOS could be explained by the inability of CCR2+ monocytes to differentiate into other CD11c+ descendants, such as interstitial macrophages (iMacs) or CD11b+ DCs, we created reporter Ccr2CreERT2/+ Tgfbr2fl/flTdTomatofl/STOP/+ and Ccr2CreERT2/+ Tgfbr2+/+TdTomatofl/STOP/+ mice to conduct fate-mapping studies. The gene discussed is MAP6; the disease is Buschke-Ollendorff syndrome.