Increased Ca2+ concentration in diabetes, including DN and diabetic neuralgia, has been attributed to numerous factors: abnormalities in the expression and physiology of Ca2+ channels, the aberrant work of sodium–potassium pump (Na+/K+-ATPase) that modulates the activity of NCX [60], impaired endoplasmic reticulum rapid Ca2+ release and maintaining, increased activity of N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionicacid (AMPA)/kainite receptors and altered extrusion systems work (plasmalemmal Ca2+-ATPase pump and Na+/Ca2+ exchanger (NCX)) [12,59]. Here, TLX2 is linked to diabetes mellitus.