Curiously, although the PI3K inhibitor had no effect on HDAC6 expression, it blocked c-myc expression (Figure 5A), suggesting that K-ras induced c-myc expression could be regulated by HDAC6 and PI3K pathways independently, or that both HDAC6 and PI3K contribute to c-myc induction and therefore tumor cell growth. The gene discussed is KRAS; the disease is neoplasm.