We believe that AT101 should be reconsidered as a viable clinical tool, with the understanding that (1) AT101 must be combined with another compound that synergizes with NOXA induction; (2) pharmacokinetic (PK) measurements will not predict AT101 efficacy in tumors as the protein continues to increase long after AT101 is removed; and (3) the induction of NOXA in the tumor should be assessed as a clinical biomarker of AT101. This evidence concerns the gene PMAIP1 and neoplasm.