Similarly, a solid variant and a less differentiated phenotype were observed in RET/PTC1 knockout for the cl2/ccdc80 gene [18], while ATCs were developed by thyroid-specific inactivation of p53 and Pten [19], or thyroid-specific combined mutations of BRAFV600E and PIK3CAH1047R [20], confirming the multi-step carcinogenesis model. The gene discussed is RET; the disease is Ehlers-Danlos syndrome, musculocontractural type.