At each RA concentration, the cancer cell growth outcome seems to reflect the combined effects of both the ‘absence’ of epigenetic transcriptional activation of RARA-targets (e.g. tumor suppressor functions like RARB2 and TGFBR2) and activation of PI3K kinase effectors (e.g. P-AKT). The gene discussed is AKT1; the disease is neoplasm.