EPCs of DM type 1 mice showed cross-talk between SHH and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/AKT pathways, which decreased the activity of AKT and increased GSK-3β activity, resulting in the degradation of the SHH pathway transcription factor GLI1/GLI2 [57]. The gene discussed is AKT1; the disease is diabetes mellitus.