My career path has experienced unconventional twists. Consequently, I have never formally held an assistant professorship in any academic institution. I conducted my Ph.D. research in copper amine oxidase structural studies with Dr. Judith P. Klinman at the University of California, Berkeley. Subsequently, I was a Damon Runyon Postdoctoral Fellow and worked in the research field of human nucleotide excision repair with Dr. Aziz Sancar at the University of North Carolina at Chapel Hill. After postdoctoral training, I first moved into the private biotech sector to search for novel amplified human oncogenes as drug discovery targets. After six years in industry, I moved back to an academic research institution, Cold Spring Harbor Laboratory (CSHL) in New York, to pursue cancer genomic research. At CSHL, my genomic research led to the discovery of a frequently amplified chromosomal region in non-small cell lung cancer. This amplification at 14q13.3 increases the gene dosage of a number of genes, including TTF-1 (thyroid transcription factor 1; also known as NKX2-1), which is a master regulator of lung development. Following this discovery, I chose to take the research program toward a different direction, i.e. mapping the connections between TTF-1 and microRNA-based signaling networks. The rationale was that the identification of microRNAs interacting with TTF-1 should present novel entry points to investigate the biology connected with TTF-1. Consequently, my laboratory discovered the first microRNA (miR-365) that directly regulates TTF-1 and the first microRNA (miR-33a) that is directly regulated by TTF-1. These findings offer new mechanistic insights into the regulation of TTF-1, which is capable of acting as either an oncogene or a tumor suppressor gene. I hope that our studies will ultimately lay the groundwork for future translational research to create TTF-1-dependent strategies to manage TTF-1-positive lung cancer.