We have previously shown that the HDACi vorinostat, in combination with the EGFR-tyrosine kinase inhibitor gefitinib, induced synergistic antitumor interaction in preclinical models of HNSCC and non-small cell lung cancer with a mechanism based, among others, on the ability of vorinostat to modulate the expression and the activity of ErbB receptors (EGFR, ErbB2, and ErbB3) (Bruzzese et al., 2011; Leone et al., 2015; Citro et al., 2019; He et al., 2019). This evidence concerns the gene ERBB3 and non-small cell lung carcinoma.