This explanation is not inconsistent with genetic data. Twin research suggests that although liabilities to addictions form two distinct groups that correspond to licit and illicit substances, each with a single additive genetic component of variance (representing variation in many genes) that accounts for most of the covariation between symptoms of abuse or dependence across respective substances, these two genetic factors are highly correlated (4). The distinctiveness of these factors is obviously not related to anything specific to the substances per se, different as they are within the groups. Rather, it is a reflection of social norms dividing the use of psychoactive substances into two categories: use of legal substances and use of illegal substances—which involves substantial norm violation. This clearly environmental factor induces different patterns of genetic relationships between and within the two substance groups. From the standpoint of this general (non-drug-specific) liability to addiction model, the pattern of drug use initiation—frequently from licit to illicit, or from “softer” to “harder” substances (but in many cases the reverse)—is variable and opportunistic, rather than uniform and developmentally deterministic (5), as posited by the “gateway hypothesis” (6). Despite that, and even though the gateway hypothesis addresses only sequential drug use initiation and does not extend to addiction disorders, the gateway hypothesis has been the foundation of many drug-related policy and research decisions. Obviously, the gateway hypothesis, which is focused on drugs per se, particularly the inconsistently defined “gateway drug”—alcohol and tobacco, or marijuana—calls for controlling the supply of that substance and the substance use behavior as such. In contrast, the general liability to addiction theory focuses on social behavior and behavior regulation precursors and concomitants of drug abuse, which is one possible developmental manifestation of socialization failure.