We speculate that the higher levels of circulating insulin in the Camkk2 WT mice, exacerbated during obesity, promote aberrant PI3K-AKT-mTOR signaling that potentially provides the missing third oncogenic piece to AVPCs previously driven by the other two genetic hallmarks of AVPC, RB1, and TP53 genetic alterations. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.