In recent research, Furmanski et al. [47] demonstrated in Gli2A mice (carrying a truncated form of Gli2 that acts as a permanent transcriptional activator of Hh target genes) that (1) GLI2A promotes Th2 differentiation (via IL4 and GATA3) in T cells, (2) Il4 is a novel target gene of Gli2-dependent Hh signaling, and (3) an allergic disease pathology was observed in house dust mite-treated Gli2A mice—showing increased eosinophil recruitment indicating enhanced inflammation, in parallel to a higher proportion of CD4+ T cells in the lung producing IL4 and IL-13, and goblet cell hyperplasia. The gene discussed is IL4; the disease is allergic disease.