It's not wrong, but (almost all) T2D arises from insulin resistance through damage to islet beta cell function. Some people with insulin resistance do not develop T2D (because they still have fully functional beta cells)
The authors admit they still need to look at T1D. They say:
"As for the limitations of this study, we cannot completely rule out the possibility that the residual endogenous islets benefitted from the surgery and acquired functional improvements. Therefore, an increase in sample size and additional trials of T1D patients with complete loss of islet β cells will help draw definitive conclusions on the causative role of E-islets in the achievement of glycemic targets."
The authors admit they still need to look at T1D. They say: "As for the limitations of this study, we cannot completely rule out the possibility that the residual endogenous islets benefitted from the surgery and acquired functional improvements. Therefore, an increase in sample size and additional trials of T1D patients with complete loss of islet β cells will help draw definitive conclusions on the causative role of E-islets in the achievement of glycemic targets."