A preclinical study showed that a reduction in PKA-Ca activity can block SCLC survival in mouse models.44 Moreover, Rb/Trp53/Rbl2 triple-knockout SCLC tumors also showed higher PKA expression compared to normal mouse lung tissue.45 Previous studies have also investigated potentially functional interactions between PKA and phosphatase 2A (PP2A).46 Inhibition of PKA or regulation of the other enzymes in the PKA signaling pathway, for example, CREB,47 may have antitumor effects in SCLC. The gene discussed is RBL2; the disease is small cell lung carcinoma.