To further confirm that BID is a general regulator of response to SAC abrogation in tumor cells, we used two approaches; (i) BID silencing with shRNA lentiviruses in two AURKBi/ TTKi-sensitive cell lines, one of them harboring the Chr22q11 amplification (NCI-H1819) and another diploid (MDA-MB-468) and (ii) BID ectopic expression with the pTRIPZ-BID vector described above in resistant cell lines of different origins and genotypes; MiaPaCa2 (KRAS G12C, pancreas), SK-MES-1 (wt for known drivers, lung squamous) and WM793 (BRAF V600E, melanoma). The gene discussed is KRAS; the disease is melanoma.