FAS and leukemia: After 1–3 h, ATM supported the phosphorylation of p53 at the level of its Ser15 residue (also reported in NB4 leukemia cells exposed to CAP 50 μM [123]) and shortly after (6–12 h) at Ser20 and 392, supporting an upregulation in the transcription and translation of the Fas/CD95 death receptor, which, after redistribution through the plasma membrane to a group with TRPV1 receptors, led to the activation of caspases 8 and 9, as well as truncated BID (tBID/p15).