Hypothetical Model of RASSF1C action in lung cancer cells: we hypothesize that RASSF1C in part activates the MEK-ERK1/2 pathway which controls a wide variety of genes that promote cell division and proliferation. The model proposes a mechanism through which RASSF1C may impact PIWIL1 expression. Since PIWIL1 is widely over-expressed in tumors compared to normal tissue, it may have important functions in cancer initiation, maintenance, or progression. PIWI-like proteins interact with PIWI-interacting RNA molecules (piRNAs) to form complexes that regulate transcriptional and translational repression leading to inhibition of apoptosis and stimulation of cell division and proliferation. Up-regulation of PIWIL1gene expression by RASSF1C is a novel and exciting discovery, suggesting a potential role for RASSF1C in early lung cancer development and progression.