be critical in this context (Yoo et al., 2011). Since Pang and colleagues showed iN cell induction by Neurod1, Ascl1, Myt1l, and Brn2, it appears that the miRNAs are able to replace the transcription factor Brn2 (Pang et al., 2011). This idea was not tested directly, however, and it is possible that the miRNAs work through yet another mechanism. More recently, another group also found miR-124 to be beneficial for human iN cell formation (Ambasudhan et al., 2011). In this report the miRNA was combined with BRN2 and MYT1L, further supporting the idea the miRNAs have a complementary function to Brn2. Surprisingly, no bHLH transcription factors were used in the latter report, but also the cells appeared less completely reprogrammed based on the absence of convincing evidence for synaptic competence. Future studies on the miRNA-transcription factor interplay responsible for iN cell formation could also be relevant to regular neural development. Thus, this extremely non-physiological method of reprogramming could perhaps even become a discovery tool for understanding normal development.
