For example, PKA may inhibit the activity of mTORC1, an important tumor-promoter, through phosphorylating the mTORC1 component Raptor on Ser791 residue [4, 151]. It warrants further studies to determine whether targeting cAMP–PKA–CREB pathway is a feasible strategy to treat cancer and reverse cancer drug resistance. The gene discussed is RPTOR; the disease is neoplasm.