Systemic inhibition of Myc in both the well-established LSL–KrasG12D murine model of non-small cell lung cancer [46] and the RIP1-Tag2 model of pancreatic insulinomas driven by SV40 T/t antigens [47] triggered rapid and wholesale regression of incipient and established tumors [48] [49], confirming that endogenous Myc function is required for maintenance of tumors driven by diverse oncogenic mechanisms. This evidence concerns the gene MYC and non-small cell lung carcinoma.