Indeed, toxic effects associated with on‐target inhibition of PI3Kα, such as hyperglycemia (Bendell et al, 2012), and the related compensatory release of insulin by the pancreas, that in turn can promote resistance to PI3K inhibition by reactivation of insulin signaling in cancer cells (Hopkins et al, 2018), may be limited by the specific targeting of the β isoform of PI3K. This evidence concerns the gene INS and cancer.