TP53 mutation are frequently found in almost 50% of tumor patients.300 These mutations either disrupt the binding to DNA or destabilize p53, and eventually attenuation of p53 function in transcription regulation.301,302 Generally loss of function of tumor suppressors is difficult to target directly, by alternative synthetic lethal strategies are readily employed in these conditions, which is exemplified by ATR or WEE1 inhibitors in TP53 deficient tumors. Here, WEE1 is linked to neoplasm.