Given that NPM1 does not appear to be a critical target for CIGB-300 in AML cells, and considering that direct enzyme inhibition has been pointed out as a parallel mechanism for the peptide in NSCLC and T-ALL cells [33,34], we carried out pull-down experiments followed by immunodetection of the CK2α catalytic subunit. The gene discussed is NPM1; the disease is non-small cell lung carcinoma.