Significance The MYC axis is commonly disrupted in cancer, mostly by activation of the MYC oncogenes but also by genetic inactivation of MAX, the obligate partner of MYC, and of the MAX partner MGA, both of which are members of the polycomb repressive complex ncPRC1.6. While the oncogenic properties of the MYC family have been extensively studied, those of the MAX-deficient cells and the role of MGA in MAX mutant cells remain unclear. In this study, we demonstrate that MAX-deficient SCLCs cells have either ASCL1 or NEUROD1 or combined characteristics. Furthermore, our data reveal that the lack of available MAX restricts MGA occupancy in gene promoters and, although the ncPRC1.6 can still be formed, there is a deficient ncPRC1.6-mediated gene repression.