EGFR and neoplasm: In parallel, it has been widely described that, upon conditions of genotoxic stress in the cellular context, presence of functional TP53 germline variants, especially hypomorphic variants (c.1010G>A), leads to a loss of p53 tumor-suppressive functions (such as DNA damage repair and cell-cycle arrest), triggering a genomic instability that, in turn, may promote the accumulation of somatic mutations at different genes (Zerdoumi et al., 2017; Park et al., 2018), which could include the hotspot regions of somatic EGFR mutations.