In the proper context, therefore, simultaneous inhibition of both TGFβ and Hh signaling by a single agent, used alone or in combination with other drugs (i.e., cytotoxic or targeted therapies), could yield significant therapeutic benefits in NSCLC across a wide range of mutational profiles [17,18] by targeting both tumor cells, as well as the tumor microenvironment [3,19]. The gene discussed is TGFB1; the disease is neoplasm.