The liaison between MYC and ATR/CHK1 may extend beyond tumors bearing genomic rearrangements of the MYC locus; in non-small cell lung cancer (NSCLC) the loss of the tumor suppressor PPP2R2A, which inhibits MYC translation, leads to high MYC activity and determines sensitivity to ATR or CHK1 inhibitors due to acute RS responses [111]. This evidence concerns the gene ATR and non-small cell lung carcinoma.