The results obtained in this study confirm the overexpression of miR-155-5p in T2D and that NTZ could modulate the effects of miR-155-5p in PBMCs by repressing inositol-polyphosphate 5-phosphatase1 (SHIP1) or via the suppressor of cytokine signaling 1 (SOCS1), attenuating the activity of NF-κB and avoiding a proliferative state, which are crucial in the development of the immune response [67] and in the synthesis of immune effector molecules, e.g., cytokines. Here, SOCS1 is linked to type 2 diabetes mellitus.