This prompted us to hypothesize whether the distinct mutational landscape, marked by the different mutations in KRAS, SMAD4, TP53 and CDKN2A (Table 2) could explain the different responses of the two human PDAC organoids to Atezolizumab stimulation, as studies are trying to understand the tumor heterogeneity in the response of patients to Immune Checkpoint Inhibitors (ICIs) treatment [53]. The gene discussed is TP53; the disease is neoplasm.