Mosaically introduced of RasG12V mutation in larval skins ubiquitously expressing TP53R175H efficiently generated tumour-like cell masses (Fig. 6a), in which γH2AX, ROS, and il1b were detected in cells with and without RasG12V mutation (Supplementary Fig. 12a–c); this cell mass formation was supressed by il1b MO or NAC treatment (Fig. 6b, c), suggesting that a newly generated RasG12V mutation can prime tumorigenesis by inducing Il1b-mediated proliferation and ROS-mediated senescence in its neighbours in the epithelia with abnormal TP53 activity. This evidence concerns the gene IL1B and neoplasm.