The results of clinical studies targeting PIP4Ks are promising, but this strategy may not be appropriate for all cancers.[36] In a recent study, the selective and potent PIP4K2A inhibitors (BAY‐091 and BAY‐297) developed by Bayer did not induce an antiproliferative effect on p53 null tumor cells, suggesting that PIP4K inhibitors must potently inhibit both PIP4K2A and other PIP4K isoforms to exert an antitumor effect.[46] Thus, attenuation of the antitumor effect of PIP4K2A inhibitors may be related to the splicing variants produced by alternative splicing. This evidence concerns the gene TP53 and neoplasm.