In that regard, in vitro work [10,14,30] suggests that thyroid cancer re-differentiation with RA requires both intact RA receptor (RAR) expression and pathways in target cells: to respond to retinoid therapy with suppressed proliferation and increased apoptosis, a cell must express the RAR isoforms, RARβ and RXRγ. This evidence concerns the gene RARB and thyroid gland carcinoma.