This study demonstrates that misexpression of RBFOX2 causes significant changes in alternative splicing that leads to dysfunctional β cells, and RBFOX2 binding is sensitive to RBFOX2 concentration26, we hypothesize that restoring normal levels of RBFOX2 expression may resolve aberrant splicing leading to disrupted insulin secretion that is observed in T2D. This evidence concerns the gene INS and type 2 diabetes mellitus.